Afferent renal nerve-dependent hypertension following acute renal artery stenosis in the conscious rat.
Anatomical and electrophysiological evidence indicates that the kidneys contain both mechano- and chemoreceptor nerve endings. We conducted the present study to determine whether conditions of reduced renal blood flow elicit cardiovascular alterations that are dependent on afferent renal nerves. Removal of the renin-angiotensin system with the angiotensin I-converting enzyme inhibitor, captopril, and/or reduction in baroreflex gain by sinoaortic denervation, were combined in conscious rats with acute renal artery stenosis to prevent these systems from potentially obscuring any afferent renal nerve-dependent effects. One week after sinoaortic denervation or sham sinoaortic denervation, each rat was chronically instrumented with Doppler flow probes on the lower abdominal aorta and superior mesenteric and right renal arteries, as well as with intravascular catheters, and a perivascular balloon occluder on the right renal artery. After surgical recovery, sham sinoaortic-denervated animals responded to a 60-minute period of stenosis (50% reduction in renal blood flow) with increases in arterial pressure, regional resistance, and plasma renin activity. Captopril abolished the increases in arterial pressure, hindquarters, and left renal resistance, but both bradycardia and increased mesenteric resistance persisted, indicating that baroreflex activation might be buffering a non-renin-angiotensin system pro-hypertensive mechanism. In support of this, sinoaortic-denervated animals during captopril administration responded to stenosis with substantial increases in arterial pressure (25-30 mm Hg) and regional resistance (30-50%) that were unrelated to the renin-angiotensin system, but which were abolished after denervation of the stenotic kidney. The data suggest that acute reductions in renal blood flow activate an afferent renal nerve-dependent cardiovascular response that is strongly expressed under conditions of reduced gain of the renin-angiotensin and baroreflex systems. We speculate that this reflex may assume particular importance in chronic renal hypertension when baroreflexes become impaired and activation of the renin-angiotensin system is reduced.
D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D001011:Aorta / Q000294:innervation; D002216:Captopril / Q000494:pharmacology; D002346:Carotid Sinus / Q000294:innervation; D003714:Denervation; D006439:Hemodynamics / Q000187:drug effects; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation*; D008297:Male; D009475:Neurons, Afferent / Q000503:physiopathology*; D011311:Pressoreceptors / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D011945:Receptors, Angiotensin / Q000187:drug effects; D012078:Renal Artery Obstruction / Q000503:physiopathology; D012084:Renin-Angiotensin System
D000806:Angiotensin-Converting Enzyme Inhibitors; D011945:Receptors, Angiotensin; D002216:Captopril