AJP - Renal Physiology, Vol 251, Issue 6 1096-F1100, Copyright © 1986 by American Physiological Society
Enhanced cAMP response to vasopressin in the CCT of DOCA-Na hypertensive rats
W. A. Pettinger, R. Fallet, Y. Wang, L. T. Tam and W. B. Jeffries
We characterized altered adenosine 3',5'-cyclic monophosphate (cAMP)
regulation in deoxycorticosterone acetate (DOCA)-Na hypertensive rats using
endogenous cAMP accumulation in the intact cell system of microdissected
renal tubule fragments. Increased cAMP accumulation in response to
vasopressin (VP) in cortical collecting tubules (CCT) began on day 5 (67%)
after exposure to DOCA-Na and increased by 320% on day 42. Increased blood
pressure began after day 7 and polyuria after day 17. The increased
response to VP was DOCA dependent and appears to be exaggerated by dietary
NaCl. Anatomic and hormone specificity studies were done on days 21-30.
These included cAMP responses to prostaglandin E2, parathyroid hormone,
thyrocalcitonin, VP, and isoproterenol in the CCT. The cAMP response to VP
was measured in the glomerulus, proximal convoluted tubule, thin descending
limb of Henle, medullary thick ascending limb of Henle, cortical thick
ascending limb of Henle, medullary collecting tubule, and CCT. The
supersensitivity occurred only to VP and only in the CCT. Thus this
alteration in the VP response is anatomic and hormone specific and does not
appear to be an acute effect of DOCA, since it was not present on day 1 and
on day 3 of DOCA exposure. DOCA-Na hypertension is VP dependent. A specific
exaggerated cAMP response to this hormone in the CCT would be expected to
cause increased sodium retention. Whether increased sodium retention at
this site contributes to hypertension in the DOCA-Na rat is unknown.
