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Captopril renography was utilized to assess the presence of angiotensin II dependent renovascular dysfunction in (1) 28 patients with mild to moderate essential hypertension (EH) with unimpaired renal function, and (2) 25 hypertensive patients with diabetic nephropathy (HDN). These studies were classified according to the diagnostic criteria outlined by the Working Party on Diagnostic Criteria of Renovascular Hypertension with Captopril Renography and the mean parenchymal transit time (MPTT) was used as an index for detecting the presence of angiotensin II dependent renal haemodynamic change. Patients with EH showed non-significant or non-specific alterations in the MPTT. Four patients in the HDN group showed a significant prolongation of MPTT in the presence of renin-angiotensin-aldosterone activation due to renal artery stenosis, and the other patients in this group showed a significant decrease in MPTT after captopril, consistent with increased blood flow and improved tubular transport function in the presence of microangiopathy only. We conclude that addition of MPTT to the standard diagnostic criteria of captopril renography may be helpful in predicting the beneficial or detrimental impact of angiotensin II inhibition treatment in HDN and in limiting the test protocol in EH to one post-captopril study.

A placebo-controlled study of Ramipril on total and intrarenal flow distribution was carried out in 7 patients with essential hypertension. Cortical nephron flow was measured using radiolabelled tubular secreted radiopharmaceuticals 123I orthoidohippurate or 99mTc mercaptoacetyl triglycine by the transit time distribution technique. Both systolic and diastolic blood pressure were reduced significantly by Ramipril without significant changes in an index of cardiac output or in effective renal plasma flow. Cortical nephron flow increased from 207 +/- 7 to 257 +/- 21 ml/min (mean +/- SEM) p less than 0.05 and the percentage of flow to cortical nephrons increased by 6% (p = 0.05). Ramipril corrects the reduced cortical nephron flow found in essential hypertension.

Nineteen patients with unilateral cerebrovascular disease underwent cerebral blood flow (CBF) measurements; ten had been receiving conventional therapy and then were studied after treatment with captopril without or with a diuretic and nine on conventional therapy were studied twice as a control group. CBF (ml min-1) was measured after an intravenous injection of 99Tcm-labelled patient's red cells with a computer linked gamma camera over the vertex and a probe over the aorta. With deconvolution analysis regional CBF is given by regional cerebral volume divided by regional mean transit time. Results in the captopril group showed on average a 10% fall in mean blood pressure and a 10% rise in blood flow to the affected hemisphere. In the control group there was on average a 4% fall in pressure, together with an 11% fall in CBF to the affected hemisphere. Captopril appears to maintain autoregulation in cerebrovascular disease.

It was considered that the first dose reaction occurring with prazosin may have been due either to hypotension or to a specific reduction in cerebral blood flow. The development of a quantitative non-invasion nuclear medicine technique for cerebral flow has now made it possible to investigate the effects of prazosin on cerebral blood flow in hypertensive patients. This double-blind study showed a significant decrease in BP and a small just significant increase in cerebral blood flow following a single 1-mg dose of prazosin, when compared with a placebo. From these results, it is unlikely that the first dose reactions which occurred with prazosin were due to a specific reduction in cerebral blood flow.