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#instalacje #ogrzewanie
COP Jest to stosunek:
ilości uzyskanej energii użytecznej (np. ciepła do ogrzewania),
do energii włożonej – napędowej (np. energia elektryczna do zasilania sprężarki).
COP (ang. coefficent of performance):
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Vasopressin regulates water excretion by increasing the water permeability of the collecting duct
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he V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] <span>Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalize

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri




Flashcard 1421579521292

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#instalacje #ogrzewanie
Question
COP Jest to stosunek:
ilości uzyskanej energii użytecznej (np. ciepła do [...]),
do energii włożonej – napędowej (np. energia elektryczna do zasilania sprężarki).
COP (ang. coefficent of performance):
Answer
ogrzewania

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COP Jest to stosunek: ilości uzyskanej energii użytecznej (np. ciepła do ogrzewania), do energii włożonej – napędowej (np. energia elektryczna do zasilania sprężarki). COP (ang. coefficent of performance):

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Ciepło jest to forma wewnętrznej energii substancji.
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Co to jest ciepło ? Ciepło jest to forma wewnętrznej energii substancji. Substancje zawierają energię cieplną, aż do temperatury zera absolutnego (0 K = -273,15°C). Nawet powietrze o temperaturze -20°C zawiera ciepło, które mogą efektywnie wykorzystywać

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Flashcard 1421581880588

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#b21 #instalacje #ogrzewanie #seo
Question
Parowanie i skraplanie odbywa się przy [...] ciśnieniu
Answer
stałym

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Parowanie i skraplanie odbywa się przy stałym ciśnieniu

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Flashcard 1421582929164

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#instalacje #ogrzewanie
Question
entalpia to zawartość [...]
Answer
energii

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entalpia to zawartość energii

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Flashcard 1421583977740

Tags
#instalacje #ogrzewanie
Question
[...] to zawartość energii
Answer
entalpia

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entalpia to zawartość energii

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#b21 #instalacje #ogrzewanie #seo
Im mniejsza jest różnica temperatur pomiędzy temperaturą zasilania obiegu grzewczego i temperaturą wejściową źródła ciepła (∆T), tym wyższy jest współczynnik wydajności COP (efektywności).
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Im mniejsza jest różnica temperatur pomiędzy temperaturą zasilania obiegu grzewczego i temperaturą wejściową źródła ciepła (∆T), tym wyższy jest współczynnik wydajności COP (efektywności). temperatura zasilania ogrzewania niższa o 1 K – COP wyższy o 2,5% temperatura źródła, np. solanki, wyższa o 1 K – COP wyższy o 2,7%

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Emma Kalanikaumaka ʻ amano Kaleleonālani Na ʻ ea Rooke of Hawai ʻ i
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Queen Emma of Hawaii - Wikipedia
eleokalani (Anglican) House Kamehameha Father High Chief George Naʻea Thomas Rooke (hānai) Mother High Chiefess Fanny Kekelaokalani Young High Chiefess Grace Kamaʻikuʻi Young Rooke (hānai) Religion Church of Hawaii Signature [imagelink] <span>Emma Kalanikaumakaʻamano Kaleleonālani Naʻea Rooke of Hawaiʻi (January 2, 1836 – April 25, 1885) was queen consort of King Kamehameha IV from 1856 to his death in 1863. She ran for ruling monarch against King Kalākaua but was defeated. Cont




#has-images

Emma was born on January 2, 1836 in Honolulu and was often called Emalani ("royal Emma"). Her father was High Chief George Na ʻ ea and her mother was High Chiefess Fanny Kekelaokalani Young.[3] She was adopted under the Hawaiian tradition of hānai by her childless maternal aunt, chiefess Grace Kama ʻ iku ʻ i Young Rooke, and her husband, Dr. Thomas C. B. Rooke.

Emma's father Na ʻ ea was the son of High Chief Kamaunu and High Chiefess Kukaeleiki.[4] Kukaeleiki was daughter of Kalauawa, a Kaua ʻ i noble, and she was a cousin of Queen Keōpūolani, the most sacred wife of Kamehameha I. Among Na ʻ ea's more notable ancestors were Kalanawa ʻ a, a high chief of O ʻ ahu, and High Chiefess Kuaenaokalani, who held the sacred kapu rank of Kekapupo ʻ oho ʻ olewaikala (so sacred that she could not be exposed to the sun except at dawn).[5]:4

[imagelink] Emma and her hānai parents.

On her mother's side, Emma was the granddaughter of John Young, Kamehameha I's British-born military advisor known as High Chief Olohana, and Princess Ka ʻ ōana ʻ eha Kuamo ʻ o.[6] Her maternal grandmother, Ka ʻ ōana ʻ eha, was generally called the niece of Kamehameha I. Chiefess Ka ʻ ōana ʻ eha's father is disputed; some say she was the daughter of Prince Keli ʻ imaika ʻ i, the only full brother of Kamehameha; others state Ka ʻ ōana ʻ eha's father was High Chief Kalaipaihala.[7][8] This confusion is due to the fact that High Chiefess Kaliko ʻ okalani, the mother of Ka ʻ ōana ʻ eha, married both to Keli ʻ imaika ʻ i and to Kalaipaihala. Through High Chief Kalaipaihala, she could be descended from Kalani ʻ opu ʻ u, King of Hawaii before Kīwalaʻō and Kamehameha. King Kalākaua and Queen Lili ʻ uokalani criticized Queen Emma's claim of descent from Kamehameha's brother, supporting the latter theory of descent. Lili ʻ uokalani claimed that Keli ʻ imaika ʻ i had no children, and that Kiilaweau, Keli ʻ imaika ʻ i's first wife, was a man.[9]:404 This was to strengthen their claim to the throne, since their great-grandfather was Kamehameha I's first cousin. But even through the second theory Queen Emma would still have been descendant of Kamehameha I's first cousin since Kalani ʻ opu ʻ u was the uncle of Kamehameha I.[5]

...
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Emma became engaged to the king of Hawaii, Alexander Liholiho. At the engagement party, a Hawaiian charged that Emma's Caucasian blood made her unfit to be the Hawaiian queen and her lineage was not suitable enough to be Alexander Liholiho's bride; she broke into tears and the king was infuriated. On June 19, 1856, she married Alexander Liholiho, who a year earlier had assumed the throne as Kamehameha IV. He was also fluent in both Hawaiian and English. Each nation and even the Chinese hosted balls and celebrations in honor of the newlyweds. Two years later on May 20, 1858 Emma gave birth to a son, Prince Albert Edward Kamehameha.

During her reign, the queen tended palace affairs, including the expansion of the palace library. During her reign and after, she was known for her humanitarian efforts. Inspired by her adoptive father's work, she encouraged her husband to establish a public hospital to help the Native Hawaiians who were in decline due to foreign-borne diseases like smallpox. In 1859, Emma established Queen's Hospital and visited patients there almost daily whenever she was in residence in Honolulu. It is now called the Queen's Medical Center.

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Queen Emma of Hawaii - Wikipedia
talents as a vocalist, pianist and dancer were well known. She was also a skilled equestrian. Married life and reign[edit] [imagelink] Emma and Queen Victoria silver christening cup [imagelink] Emma and Kamehameha IV <span>Emma became engaged to the king of Hawaii, Alexander Liholiho. At the engagement party, a Hawaiian charged that Emma's Caucasian blood made her unfit to be the Hawaiian queen and her lineage was not suitable enough to be Alexander Liholiho's bride; she broke into tears and the king was infuriated. On June 19, 1856, she married Alexander Liholiho, who a year earlier had assumed the throne as Kamehameha IV. He was also fluent in both Hawaiian and English. Each nation and even the Chinese hosted balls and celebrations in honor of the newlyweds. Two years later on May 20, 1858 Emma gave birth to a son, Prince Albert Edward Kamehameha. During her reign, the queen tended palace affairs, including the expansion of the palace library. During her reign and after, she was known for her humanitarian efforts. Inspired by her adoptive father's work, she encouraged her husband to establish a public hospital to help the Native Hawaiians who were in decline due to foreign-borne diseases like smallpox. In 1859, Emma established Queen's Hospital and visited patients there almost daily whenever she was in residence in Honolulu. It is now called the Queen's Medical Center. Prince Albert, who was always called "Baby" by Emma, had been celebrated for days at his birth and every public appearance. Mary Allen, wife of the Chief Justice of the Supr




Flashcard 1421603638540

Question
[...] regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct
Answer
Vasopressin

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Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct

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Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri







Flashcard 1421604687116

Question
[...] regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct
Answer
Vasopressin

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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scheduled repetition interval               last repetition or drill

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Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri







Flashcard 1421606522124

Question
[...] regulates water excretion by increasing the water permeability of the collecting duct
Answer
Vasopressin

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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Vasopressin regulates water excretion by increasing the water permeability of the collecting duct

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri







Flashcard 1421607570700

Question
[default - edit me]
Answer
increasing the water permeability

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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scheduled repetition interval               last repetition or drill

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Vasopressin regulates water excretion by increasing the water permeability of the collecting duct

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri







Flashcard 1421608881420

Question
[default - edit me]
Answer
increasing the water permeability

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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Vasopressin regulates water excretion by increasing the water permeability of the collecting duct

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri







Flashcard 1421609929996

Question
[...] part of the G protein of M2 can open K+ channels, which slows down the heart rate
Answer
G-Beta-gamma

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G-Beta-gamma part of the G protein of M 2 can open K + channels, which slows down the heart rate

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Muscarinic acetylcholine receptor M2 - Wikipedia
is claim instead found no significant association between the CHRM2 gene and intelligence. [8] Olfactory behavior[edit] Mediating olfactory guided behaviors (e.g. odor discrimination, aggression, mating) [9] Mechanism of action[edit] <span>M 2 muscarinic receptors act via a G i type receptor, which causes a decrease in cAMP in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors. [10] In addition, they modulate muscarinic potassium channels. [11] [12] In the heart, this contributes to a decreased heart rate. They do so by the G beta gamma subunit of the G protein coupled to M 2 . This part of the G protein can open K + channels in the parasympathetic notches in the heart, which causes an outward current of potassium, which slows down the heart rate. Ligands[edit] Few highly selective M 2 agonists are available at present, although there are several non-selective muscarinic agonists that stimulate M 2 , and a number of selectiv







Flashcard 1421610978572

Question
[...] regulates water excretion by increasing the water permeability of the collecting duct
Answer
Vasopressin

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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Vasopressin regulates water excretion by increasing the water permeability of the collecting duct

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri







Flashcard 1421612289292

Question
[...] regulates water excretion by increasing the water permeability of the collecting duct
Answer
Vasopressin

statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

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Vasopressin regulates water excretion by increasing the water permeability of the collecting duct

Original toplevel document

Vasopressin receptor - Wikipedia
luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. [1] V 2 receptor[edit] <span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. [1] The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s . [3] The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. [1] V 3 receptor[edit] The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri