To study if the severity of hypertension could be associated with disturbances of the autoregulation of renal blood flow and glomerular filtration, we compared the renal hemodynamic and functional responses to acute blood pressure reductions of a group of patients with moderate essential hypertension (n=10) with those of a group of patients with severe hypertension (n=10). Blood pressure was reduced to normal levels by a stepwise infusion of sodium nitroprusside, and effective renal blood flow (by 131 I-hippuran), glomerular filtration rate (by endogenous creatinine clearance), and filtration fraction were determined. After acute blood pressure normalization, effective renal blood flow and glomerular filtration rate were significantly reduced in patients with severe hypertension (-41.6±8J% and -44.7±6.8%, respectively,/><0.01 for both) but not in those with moderate hypertension (+4.9±9.1% and +62±133%, respectively, NS). Filtration fraction remained unchanged in both groups. These results show that severe but not moderate essential hypertensive patients have a displacement to the right of the lower limit of the renal autoregulation curve due to impaired vasodilation to maintain adequate renal blood flow during acute reductions of blood pressure. This impairment may be due to anatomic or functional defects of preglomerular vessels, or to both. Furthermore, the inability to maintain adequate glomerular filtration in these circumstances shows that patients with severe hypertension also have an impaired ability to adjust postglomerular vasomotor tone in the face of reductions in glomerular blood flow. (Hypertension

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To test the ability of the hypertrophied ventricle to increase its contractility in response to sympathetic stimulation, we compared the chronotropic, inotropic, and relaxation responses to graded in fusions of isoproterenol in spontaneously hypertensive rats (SHR) with responses of matched Wistar-Kyoto (WKY) controls. A closed-chested, direct ventricle puncture was used for the study. The SHR required a higher threshold dose (0.04 vs 0.01 micrograms/kg/min) for a significant chronotropic response, and their maximal response of heart rate was smaller than in WKY (delta HR = +12.5 +/- 5.4 vs +22.8 +/- 10.7 beats/min, p less than 0.01). Contractility indices did not increase in the SHR after isoproterenol infusion: (delta dP/dt +2224.3 +/- 1304.7 mm Hg/sec; delta dP/dt/P = +5.1 +/- 9.3 sec-1, p greater than 0.05) in sharp contrast with the marked increases observed in WKY (delta dP/dt = +4682.1 +/- 435.0 mm Hg/sec, p less than 0.01; delta dP/dt/P +78.6 +/- 8.0 sec-1, p less than 0.001). Left ventricular relaxation rate was marked diminished by isoproterenol in SHR (delta neg dP/dt = -2598.6 +/- 855.0 mm Hg/sec) whereas it was not altered significantly in normotensive rats. Thus, cardiac contractile and chronotropic responses were markedly diminished in SHR, possibly as a result of diminished beta adrenoreceptor mediation; further, the impairment of the relaxation rate induced by isoproterenol in SHR might also interfere with contractile cardiac performance during stress.

We examined the hemodynamic features of 24 untreated patients with surgically proven pheochromocytoma during steady-state periods and compared them with 24 untreated essential hypertensive patients individually matched for sex, age, body surface area, and arterial blood pressure. We found that, despite having 10-fold higher levels of circulating catecholamines, pheochromocytoma patients have hemodynamic characteristics similar to patients with essential hypertension and that, in individual patients, the ratio of circulating norepinephrine to epinephrine had no relation to the hemodynamic profile. In both groups, increased total peripheral resistance is primarily responsible for maintenance of hypertension. These results suggest that, unlike the acute administration of catecholamines, long-term exposure to high levels of circulating catecholamines does not produce hemodynamic responses characteristic of this group of compounds. This might be due in part to desensitizatlon of the cardiovascular system to catecholamines and might explain the clinical observation that some patients can be completely asymptomatic despite harboring an actively catecholamine-secreting pheochromocytoma. (Hypertension 1990;15(suppl I):M28-I-131)