To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E 2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E 2 concentration in renal venous plasma from the stenotic kidney was 9.25 ±1.48 pg/ml, which was significantly higher (/?<0.01) than the concentration in the renal venous plasma from the normal kidney (4.97±1.02 pg/ml) or in the aortic plasma (2.59±0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E 2 correlated significantly with a renin ratio greater than 1.5 (r=0.8211, p<0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E 2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120±6 to 110±5 mm Hg,p<0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (/?<0.05) and in the renal vein of the stenotic kidney (/?<0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure. These data indicate that renal prostaglandin plays an important role in the augmented release of renal renin and the pathogenesis of hypertension in human renovascular hypertension. {Hypertension 1989;14:461-468)

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The minimum degree of renal arterial stenosis needed to cause hypertension was identified by renal arterial angiography of anesthetized dogs. The effects of renal nerves and prostanoids on the critical stenosis were also examined. The left renal artery was constricted concentrically by a radiolucent constrictor device, and the stenosis of the artery was evaluated by cineangiography with the kidney either innervated or denervated. At this time, renal blood flow, renal perfusion pressure, and systemic blood pressure were serially monitored. In another group of dogs, renal venous and aortic blood samples were taken as the stenosis increased; these were assayed for prostaglandin E2 and plasma renin activity. The same experiments were done again after treatment with a cyclooxygenase inhibitor, aspirin DL-lysine (54 mg/kg). With the kidney either innervated or denervated, systemic blood pressure began to increase when the stenosis was more than 70% of the diameter of the renal artery; the renal blood flow decreased when the stenosis was more than 75% of the diameter. Aspirin treatment attenuated the increase in blood pressure but did not affect the autoregulation of the renal blood flow when stenosis was 70% or less. Prostaglandin E2 production increased in the stenotic kidney when the stenosis was more than 70%; aspirin inhibited prostaglandin synthesis and suppressed the stimulation of renin release. These results suggest that whether there is innervation or not, the critical degree of renal arterial stenosis that causes hypertension is more than about 70% of the diameter in the presence of renal prostaglandins; in their absence, the critical point above which hypertension occurs is 75% or more.

SUMMARY Cardiovascular hemodynamics (microspheres) and plasma norepinephrine and epinephrine levels at rest and during short-term shaker stress were investigated in conscious spontaneously hypertensive rats and Wistar-Kyoto rats, with or without oral taurine (1.5%) treatment for 8 weeks. Taurine effects were evaluated by comparing data on the taurine-treated and untreated rats. Taurine affected neither the resting hemodynamics nor the resting plasma catecholamine levels in spontaneously hypertensive and Wistar-Kyoto rats. Taurine slightly but significantly reduced the left ventricular/body weight ratio in the spontaneously hypertensive rats (p < 0.05) and caused an insignificant 10 mm Hg decrease in the resting mean arterial pressure. Spontaneously hypertensive and Wistar-Kyoto rats responded in a qualitatively similar manner to stress, as evidenced by resistance-dominated increases in mean arterial pressure and increases in heart rate, with a blood flow redistribution from splanchnic, cutaneous, and testicular to skeletal muscle and cerebral circulations and by increases in plasma norepinephrine and epinephrine levels. These changes were more marked in the spontaneously hypertensive rats. Taurine significantly reduced the stress values of mean arterial pressure (untreated, 189 ± 4 (SE) mm Hg; treated, 166 ± 4 mm Hg in the spontaneously hypertensive rats; p < 0.05), while it significantly reduced stress values of heart rate in spontaneously hypertensive and Wistar-Kyoto rats (p < 0.05). Taurine also blunted the stress values of splanchnic, testicular, and cutaneous vascular resistance in the spontaneously hypertensive rats. There were no or only slight regional effects in the Wistar-Kyoto rats. Taurine substantially decreased plasma levels of norepinephrine (untreated, 615 ± 76 pg/ml; treated, 383 ± 49 pg/ml) and epinephrine (untreated, 892 ± 187 pg/ml; treated, 232 ± 59 pg/ml) during stress in the spontaneously hypertensive rats. These results indicate that chronic taurine treatment attenuates short-term shaker stress-induced hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats. (Hypertension 7: 913-922, 1985) KEY WORDS • shaker stress • systemic and regional hemodynamics sympathoadrenomedullary activity P ATIENTS with essential hypertension, and even their normotensive adolescent offspring, often show hyperresponsiveness to physical and psychological stress. '• 2 Likewise, adult and young spontaneously hypertensive rats (SHR), the most ex-

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