Mechanisms in human renovascular hypertension.

Abstract

SUMMARY To clarify the pathophysiology of renovascular hypertension, we monitored intraarterial pressure continuously and measured hourly hormone levels for 24 hours under carefully controlled conditions in two hypertensive patients with unilateral renal artery occlusion. Comparison of the results with those obtained when the patients were normotensive 3 months after uninephrectomy indicated that, while the renin-angiotensin system played a central role in maintaining the hypertension, the sympathetic nervous system also contributed and, in addition, modulated short-term arterial pressure fluctuations. In the untreated state, the sympathetic regulation of renin secretion was heightened, and angiotensin H/aldosterone dose-responsiveness was augmented. It is suggested that these adaptive changes might serve to offset the tendency to severe sodium depletion and thence exacerbation of the hypertension. (Hypertension 5: 597-602, 1983) KEY WORDS • renal hypertension • renin • angiotensin • aldosterone • catecholamines T HE mechanisms underlying renal hypertension are unclear despite intensive study. For the more common form in humans -unilateral renal artery stenosis with the contralateral kidney intact (the equivalent of two-kidney, one clip hypertension in experimental animals 1 ), the renin-angiotensin system is thought to play a central role both in the development and maintenance of hypertension.2 More contentious and less researched is involvement of the sympathetic nervous system in regulating arterial pressure and controlling renin release from the ischemic kidney. Much of our knowledge linking pressure and hormone changes is based on animal experiments, but prominent species differences 3 ' 4 hamper application of these findings to humans. Previous studies in humans have tended to focus on a single pathophysiological variable -usually renin -and an integrated assessment of hormone-blood pressure relationships has not yet been undertaken. To clarify these interrelationships we monitored arterial pressure continuously, and From the

Hyponatremic-Hypertensive Syndrome With Renal Ischemia

“…As to the pathophysiology of the syndrome, the explanation provided by Atkinson et al 18 appears plausible and is supported by our previous 16 and current observations. With "critical" renal ischemia, renin secretion is increased, resulting in high circulating angiotensin II levels, which raise arterial pressure and stimulate aldosterone secretion from the adrenal glomerulosa.…”

“…The clinical and neuroendocrine features of 1 patient (No. 16, Table) have been described in detail elsewhere, 16 and details of 5 patients have been reported previously. 15,17 As in the 4 cases of Heslop et al, 15 which are included in the current report, the majority of patients were elderly, asthenic females.…”

“…Barraclough 24 partly succeeded in such an endeavor when, in 1966, he documented gross sodium, potassium, and volume depletion with the evolution of severe hypertension and hyponatremia in a patient with unilateral renal ischemia. Further, the fact that the component electrolyte and hormonal abnormalities are corrected and cumulative sodium balance increases with uninephrectomy or blockade of angiotensin II production 16,18 adds weight to the thesis outlined above.…”

Central Mineralocorticoid Receptors and the Role of Angiotensin II and Glutamate in the Paraventricular Nucleus of Rats With Angiotensin II–Induced Hypertension

“…[40][41][42] Our previous study showed that an increase in circulating Ang II activates an aldosterone-MR-EO pathway in the brain leading to sympathetic hyperactivity and hypertension.…”

“…[40][41][42] Our previous study showed that an increase in circulating Ang II activates an aldosterone-MR-EO pathway in the brain leading to sympathetic hyperactivity and hypertension. 2 The current study shows that this slow neuromodulatory pathway maintains the elevated BP from circulating Ang II by enhancing AT 1 and glutamate receptor-dependent signaling in the PVN.…”