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some questions re: angiotensin

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youngrace

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1) can aldosterone be secreted without angiotensin ii?
2) since renin secreted by the jg cells is what cleaves angiotensinogen to angiotensin 1, doesn't it take a while for angiotensin 1 to reach the lungs and be converted to angiotensin 2?
3) do the dilation effects of the macula densa on afferent arterioles override the vasoconstriction effects of angiotensin ii?

(sorry for the spam of kidney / angiotensin questions today)
 

Ssina

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1) can aldosterone be secreted without angiotensin ii?
Wiki: it is also stimulated by plasma acidosis, stretch receptors on the heart and a lipid factor
2) since renin secreted by the jg cells is what cleaves angiotensinogen to angiotensin 1, doesn't it take a while for angiotensin 1 to reach the lungs and be converted to angiotensin 2?
Wiki: "ACE),which was thought to be found mainly in lung capillaries. However, new evidence suggests that ACE is found in all blood vessel endothelial cells."
plus I don't think it would take that long for it to get to lungs once renin is released in the blood and converts the zymogen, which is already present.
3) do the dilation effects of the macula densa on afferent arterioles override the vasoconstriction effects of angiotensin ii?

(sorry for the spam of kidney / angiotensin questions today)
Ang II is more potent on the Efferent (to increase the GFR by the buildup of the blood in glomerulus) than the Afferent, but I see what you mean. I think Ang II by being more potent on Efferent together with the fact that MD vasodilate Afferent and stimulate JG to release more renin..... essentially the Efferent gets constricted way more than Afferent to maintain the GFR in the kidney due to the lower BP.

I usually associate the effect of Renin/Ang for the blood pressure increasing the Total Peripheral Resistance (through vasoconstriction of vessels throughout the body) to increase the mean arteriole pressure because of low blood volume (while your bleeding out)... essentially increasing CO and BP. And I associate MD cells with flow rate and osmolarity in the kidney, which they regulate via vasoconstriction or dilation of the afferent arteriole. But when the BP drops, JG cells (baroreceptors) senses it via pressure and MD cells (chemoreceptors) via osmolarity/[NaCl] at Distal Tubule. Then they both activate/stimulate Renin secretion for Ang II effects (JG) and vasodilation (MD cells) to increase blood pressure and maintain GFR at the kidney dynamically, rather than working against each other

at least that's my input!
 
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