Showing papers by "Suzanne Oparil published in 1993"

Normotensive blacks have heightened sympathetic response to cold pressor test.

Abstract: The purpose of this study was to compare sympathetic nerve activity responses to the cold pressor test in black and white normotensive subjects. We recorded muscle sympathetic nerve activity (microneurography of the peroneal nerve), arterial blood pressure, and heart rate in 9 normotensive American blacks (24 +/- 2 years, mean +/- SEM) and 10 normotensive American whites (28 +/- 2 years) at rest and during hand immersion in ice water (cold pressor test). Body weight was not different in the two groups (72.4 +/- 3.7 versus 74.1 +/- 3.8 kg, black versus white subjects). During supine rest, mean arterial pressure (92 +/- 2 versus 93 +/- 3 mm Hg, black versus white), heart rate (66 +/- 4 versus 62 +/- 3 beats per minute, black versus white), and muscle sympathetic nerve burst frequency (12 +/- 2 versus 17 +/- 3 bursts per minute, black versus white) were not different in the two groups. During the cold pressor test, mean arterial pressure, heart rate, and muscle sympathetic nerve activity increased from supine rest in both groups. The magnitudes of increases in mean arterial pressure and total minute muscle sympathetic nerve activity were significantly greater in blacks than whites (33.5 +/- 3 versus 22.4 +/- 3 mm Hg and 416 +/- 24% versus 243 +/- 31% of control, respectively, black versus white, P < .05). The increases in heart rate were most significantly different for the two groups. These data suggest that the enhanced pressor response to cold stress observed in normotensive blacks is attributable to greater increases in peripheral sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitric oxide mediates immune dysfunction in the spontaneously hypertensive rat.

Abstract: The immune system of the spontaneously hypertensive rat is dysfunctional compared with that of normotensive control strains. Previous studies from our laboratory have shown that immunodepression in the spontaneously hypertensive rat was mediated by macrophages. The current study examines the mechanism for the depressed proliferative responses to concanavalin A typically observed by splenic mononuclear cells of spontaneously hypertensive rats. We tested various inhibitors of known macrophage products responsible for suppressing lymphoid function. The nitric oxide synthetase inhibitor NG-monomethyl L-arginine produced dose-dependent derepression of the proliferative responses of splenic mononuclear cells to concanavalin A. In contrast, indomethacin and catalase exhibited only weak derepression of the proliferative responses. Subsequent analysis showed that splenic mononuclear cells from spontaneously hypertensive rats generated greater nitric oxide levels than cells from Wistar-Kyoto rats, and nitric oxide levels were reduced when the inhibitor was added to splenic mononuclear cell cultures from spontaneously hypertensive rats. We further demonstrated that L-arginine is required for the development of the depressed mitogen-induced proliferative responses in these cells. Addition of L-arginine in excess of 10 microM to cultures diminished cell proliferation and increased nitric oxide. Polyclonal antibodies to murine interferon gamma reduced nitric oxide accumulation by approximately 50%, suggesting that interferon gamma is partially responsible for enhancing nitric oxide production in mitogen-stimulated splenic mononuclear cell cultures from spontaneously hypertensive rats. Thus, this study provides evidence that the immune depression observed in the spontaneously hypertensive rat is nitric oxide dependent.

Antihypertensive therapy--efficacy and quality of life.

Abstract: In the 20 years since the creation of the National High Blood Pressure Education Program, remarkable progress has been made in detecting and treating hypertension in the United States1. The number ...

Coarctation induces alterations in basement membranes in the cardiovascular system.

Abstract: A coarctation hypertensive rat model was used to examine the effects of elevated blood pressure on basement membrane component synthesis by cardiac myocytes and aorta using immunohistochemistry and Northern blot analysis. Carotid arterial pressure increased immediately on coarctation, and left ventricular hypertrophy was maximal within 5 days. In immunohistochemical studies, fibronectin and laminin were increased and the basement membrane chondroitin sulfate proteoglycan decreased in both the subendothelial space and smooth muscle cell basement membranes of the aorta above the clip compared with controls, whereas only fibronectin was elevated in the aorta below the clip. No change in basement membrane staining intensity for the cardiac myocytes was observed. Alterations in steady-state mRNA levels for fibronectin and laminin in the aorta paralleled those observed by immunohistochemical analysis with regard to protein and tissue type affected as well as intensity of the changes. However, changes in mRNA levels (but not protein deposition) for perlecan and type IV collagen were also observed in aortas from hypertensive rats compared with controls. Increases in steady-state mRNA levels for all basement membrane components in the heart and vasculature peaked before maximal cardiac hypertrophy (5 days). These studies indicate that alterations in basement membrane component deposition in the hypertrophied vasculature occur at both transcriptional and translational levels and suggest that the cell attachment glycoproteins fibronectin and laminin may be important factors in the vascular response to elevated transmural pressure.

Atrial Natriuretic Factor in Central Cardiovascular Control

Abstract: A complete atrial natriuretic factor (ANF) synthetic, processing, and effector system is found in rat brain. ANF in critical brain regions, including anterior hypothalamic area and nucleus tractus solitarii, contributes importantly to the tonic control of blood pressure, sympathetic outflow, and baroreceptor reflex sensitivity in the spontaneously hypertensive rat.

Excitatory Sympathetic Reflex in NaCl-Sensitive Spontaneously Hypertensive Rats

Abstract: We have previously demonstrated blunted reflex responses of lumbar sympathetic nerve activity during volume expansion in NaCl-sensitive spontaneously hypertensive rats maintained on basal (1% NaCl) diets compared with NaCl-resistant spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats. The current study tested the hypothesis that chronic ingestion of a high (8%) NaCl diet further blunts cardiopulmonary reflex function in the NaCl-sensitive spontaneously hypertensive rat. After 3 weeks of a 1% or 8% NaCl diet, male rats of all four strains were instrumented with femoral arterial and venous cannulas and lumbar nerve recording electrodes at 10 weeks of age. Two days later, conscious rats were infused with whole blood to expand blood volume. NaCl-sensitive spontaneously hypertensive rats maintained on a 1% NaCl diet had blunted responses of nerve activity to acute volume expansion compared with control strains. NaCl-sensitive spontaneously hypertensive rats maintained on an 8% NaCl diet had increases in nerve activity responses to volume expansion. In a second experiment, the volume expansion protocol was repeated in anesthetized NaCl-sensitive spontaneously hypertensive rats that had been subjected to sinoaortic denervation after 3 weeks of a 1% or 8% NaCl diet. After sinoaortic denervation, an increase in nerve activity was again observed during volume expansion in animals fed the 8% NaCl diet. In animals fed the 1% NaCl diet, changes in nerve activity were variable. The excitatory response was significantly reduced after bilateral vagotomy. These studies suggest that blood pressure regulation in NaCl-sensitive spontaneously hypertensive rats is a complex interaction of excitatory and inhibitory sympathetic reflex systems that is altered by high dietary NaCl exposure.