Hypertension
-
Specific causes of death were analyzed for 10,908 participants in the Hypertension Detection and Follow-up Program, to explore possible explanations for the observed excess 8.3-year mortality from all causes in hypertensives with low body mass. Although the cardiovascular mortality rate among men in the lowest decile of body mass (body mass index 21.96 or less) was 50% higher than that of men in the median class (body mass index 26.4-28.8), death rate for noncardiovascular deaths was more than 2 1/2 times higher in men with lean versus median body mass. The pattern was similar among women. ⋯ There was no evidence that more severe or treatment-resistant hypertension was present in or could explain excess mortality among the hypertensives with low body mass. The inference from the findings is not that overweight is protective for hypertensives nor that excess risk is due to leanness per se. Rather, a reasonable hypothesis, particularly from findings on specific causes of death, is that excess mortality in lean hypertensives is due to deleterious lifestyles, particularly smoking and excess alcohol intake, contributing to both leanness and risk of death.
-
The modulation exerted by atrial natriuretic factor (ANF) on the cardiac and vascular influences of arterial baroreceptors was investigated in two groups of unanesthetized, chronically instrumented normotensive rats. In group 1, the reflex control of heart rate was assessed by graded baroreceptor stimulations and deactivations obtained by intravenous boluses of phenylephrine and nitroprusside. Under either circumstance, baroreceptor reflex sensitivity was expressed as the linear regression slope relating the chronotropic responses to the drug-induced mean arterial pressure changes. ⋯ ANF infusion (0.20 micrograms/kg/min) performed in further separate groups of conscious rats raised plasma ANF to 480 +/- 58 fmol/ml. Values in control vehicle-infused rats were 50 +/- 8 fmol/ml. Vascular reactivity (pressor response to intravenous phenylephrine boluses in anesthetized, sinoaortic-denervated rats) was only minimally reduced by ANF.(ABSTRACT TRUNCATED AT 250 WORDS)
-
This review considers in some detail the hypothetical relationships between sodium fluxes, both active and passive, across the cell membrane, and intracellular sodium concentration in vascular smooth muscle in the animal models of hypertension. It appears that two basic types of transport defects, increased cell membrane permeability to sodium and decreased active pumping of sodium at a given internal sodium concentration, can exist in vascular smooth muscle in experimental hypertension, and that sometimes the two defects coexist, further increasing internal sodium concentration. It is possible that eventually we may find similar transport defects in vascular smooth muscle in humans with arterial hypertension. ⋯ Future directions for research in the area are also considered. First priority should be given efforts to determine the chemical structure of the sodium pump inhibitor(s). High priority should also be given to attempts to measure passive and active sodium fluxes and intracellular sodium concentration in vascular smooth muscle cells in vivo, and to determine the role of atrial natriuretic factor in the genesis and maintenance of hypertension.
-
The effect of hypertension on patient and allograft survival in 60 diabetic recipients of transplanted kidneys was assessed by retrospective chart analysis. Hypertension was present in 81% of recipients. ⋯ At a mean of 21 months after transplantation, living hypertensive diabetic recipients had worse renal function (mean serum creatinine of 3.1 mg/dl) than did nonhypertensive recipients (mean serum creatinine of 1.6 mg/dl). It is concluded that hypertension is a significant risk factor for diabetic patients and kidneys after transplantation.
-
Conscious rabbits infused intravenously (i.v.) with isotonic saline at 1.5 to 1.8 ml/min for 24 hours had greater pressor responses to norepinephrine (NE) than did normal control rabbits. Infusion of the angiotension II (ANG II) antagonist [Sar1, Ile8] ANG II did not decrease the exaggerated pressor responses to NE in saline-infused rabbits. Measurements of cardiac output (CO) as well as the pressor responses to NE before and after saline infusion revealed that, although saline infusion increased the CO and decreased total peripheral resistance (TPR), CO did not change during NE infusion either before or after saline infusion, but NE produced significantly greater increases in mean arterial pressure (MAP) and TPR after saline infusion than before the saline infusion. ⋯ There was no evidence to indicate that ANG II was involved in the mechanisms producing this pressor hyperresponsiveness. Some circulating hormonal factor, however, was involved in mediating the pressor hyperresponsiveness following saline infusion. The results of this study are compatible with the concept that natriuretic hormone may play a role in promoting pressor hyperresponsiveness in saline-expanded animals.