Faculty Bibliography

Renal insufficiency, with serum creatinines ranging from 2.3 to 13.4 mg/dl, was observed in 15 patients with the minimal change nephrotic syndrome. Recovery of renal function occurred in association with diuretic therapy in 13, eight of whom subsequently underwent steroid-induced remission of the nephrotic syndrome. Two patients failed to undergo diuresis or to have a remission of the nephrotic syndrome and died with persistent renal failure. Glomerular filtration rate (Cinulin) was reduced out of proportion to renal plasma flow (CPAH) as evidenced by remarkably low filtration fractions ranging from 0.03 to 0.095. The invariable association between diuresis and recovery of renal function, the recurrence of renal failure when fluid reaccumulated and the finding of markedly depressed filtration fractions lead us to postulate that renal failure in minimal change nephrotic syndrome may be due to a reversible alteration in glomerular hemodynamics which is related to fluid retention and associated intrarenal edema

An organic mental syndrome developed in a patient soon after he underwent repair of a dissecting thoracic aortic aneurysm. The operation was accomplished with cardiopulmonary bypass. Initially, the mental changes were thought to be related to the operation. However, they subsequently were shown to be associated with propranolol. The potential role of propranolol in inducing central nervous system disturbances is emphasized, and the literature on the subject is reviewed

Patients undergoing surgical procedures using sodium nitroprusside-induced hypotension were studied to determine the role of the renin-angiotensin system in the pathogenesis of rebound hypertension (RH) after discontinuing sodium nitroprusside (SNP) infusion. Retrospective observations documented RH in 9 of 12 patients (group I) with a systolic blood pressure (SBP) increase from 112 +/- 3.92 before SNP to 144 +/- 5.60 torr 10 min after SNP (p less than 0.001). In 12 patients (group II), plasma renin activity (PRA) rose from 950 +/- 432 to 3,611 +/- 1.874 pg/ml/hr (p less than 0.0005) during SNP and remained elevated (2,504 +/- 792 pg/ml/hr) 30 min after cessation of SNP. SBP rose from a control (pre-SNP) value of 112 +/- 5.24 to 129 +/- 8.52 torr after discontinuation of SNP (p less than 0.05). Significant PRA and SBP changes did not occur in a matched group of patients (group III) who did not receive SNP. That RH after cessation of SNP infusion was associated with persistent elevation of PRA leads us to suggest that RH may be attributable to the unopposed effects of the renin-angiotensin system after the rapid plasma disappearance of SNP

We examined the effects of an angiotensin III (AIII) analog, isoleucine-7 AIII (Ile7-AIII), on the steroidogenic and pressor responses to angiotensin II (AII) and AIII. AII or AIII (25 ng/kg/min) were infused alone or superimposed on an infusion of Ile7-AIII (100 ng/kg/min) in conscious male New Zealand rabbits. AII and AIII induced comparable increases in plasma aldosterone concentration, but AII exhibited significantly greater pressor effect. Ile7-AIII infusion resulted in significant inhibition of AII- but not AIII-induced steroidogenesis. Despite inhibition of aldosterone production, Ile7-AIII failed to block the pressor or renin-suppressing effect of AII. Inhibition of the steroidogenic effect of AII, but not of AII, by Ile7-AIII may be taken as evidence that adrenal stimulation by AII is direct and is not mediated by in vivo conversion to the heptapeptide. The ability of the heptapeptide analog to block aldosterone stimulation by the octapeptide AII suggests that adrenal receptors may, however, have a greater affinity for the heptapeptide

Clonidine represents the prototype of a new class of centrally acting antihypertensive agents, classed as partial alpha-adrenergic antagonists. Blood pressure reduction is characterized, hemodynamically, by reduced cardiac output with unchanged peripheral vascular resistance at rest. Reflex control of blood pressure during orthostasis and exercise appears to be unimpaired, and orthostatic hypotension is uncommon. As with most other antihypertensive agents, satisfactory reduction of blood pressure with clonidine given as a sole agent is limited to patients with relatively mild hypertension; an additive or synergistic effect of diuretic administration has been well documented. Abrupt withdrawal of clinidine has been reported to be followed, within 24 to 36 h, by rebound hypertension, tachycardia, cardiac arrhythmias, and other changes suggestive of sympathetic overactivity. The incidence and clinical significance of rebound hypertension after abrupt cessation of clonidine therapy, and indeed the profile of blood pressure responses to varying physical activity during therapy, remain to be evaluated.