ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The effects of captopril and angiotensin II on adrenergic neurotransmission have been studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In a pithed rat preparation, vasoconstrictor responses evoked by spinal stimulation were greater in SHR than WKY (p< 0.01). Captopril reduced responses to electrical stimulation and this reduction was greater in the SHR (p< 0.001). Bilateral nephrectomy reduced the vasoconstrictor responses to nerve stimulation in both strains of rat and abolished the effects of captopril. In an isolated perfused mesenteric artery preparation, responses to nerve stimulation in the absence of angiotensin II were greater in SHR than WKY (p< 0.05). Angiotensin II potentiated responses from both strains of rat, however the amplitude of the potentiation was greater in preparations from the SHR than those from WKY (p< 0.002). Captopril (30/by mouth) reduced blood pressure in conscious SHR over a 5-day dosing period. In WKY rats, no hypotensive action of captopril was observed. However, in another normotensive strain, the Alderley Park Wistar rat (APW), captopril lowered blood pressure. Plasma renin activity was not significantly different among these three strains of rat. The APW have previously been shown to be very sensitive to the adrenergic potentiating actions of angiotensin II. Captopril thus lowers blood pressure in SHR and APW, and both these strains are sensitive to the adrenergic potentiating actions of angiotensin II. It does not lower blood pressure in WKY, which is relatively insensitive to these actions of the octapeptide. Therefore, the hypotensive action of captopril in the rat may be due to its interference with the adrenergic potentiating effect of angiotensin II. (Hypertension 4: 764–772, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

In stroke-prone spontaneously hypertensive rats (SHRSP) plasma norepinephrine levels and vascular reactivity to norepinephrine are increased and intravascular volume is reduced during the developmental phase of hypertension. Since the accelerated rise in blood pressure following sodium-loading in SHRSP cannot be attributed to the volume-retaining properties of sodium, the effects of an increased dietary intake of sodium on biochemical parameters of sympathetic vascular tone were investigated. The following results were obtained. First, the increased reactivity of vascular smooth muscle was further augmented in sodium-treated SHRSP; the degree of supersensitivity was positively correlated to the plasma sodium concentration. After blockade of the neuronal uptake by 30 μM cocaine, no difference in vascular reactivity to norepinephrine was detected between SHRSP on a normal and SHRSP on a high-sodium diet. Second, the inactivation of norepinephrine by the neuronal uptake was impaired in rats on a high-sodium diet, the impairment being more pronounced in SHRSP than in Wistar-Kyoto (WKY) rats. This decreased inactivation could be expected to cause higher concentrations of the neurotransmitter at the receptor site if the transmitter release from the nerve ending remains constant. Third, the release of norepinephrine and epinephrine into the plasma was increased in sodium-loaded SHRSP but not in sodium-loaded WKY. Cold exposure exaggerates these differences between normotensive and hypertensive rats. These findings suggest that a high-sodium intake modifies the transmission of sympathetic impulses at the level of the nerve terminal in both WKY and SHRSP. In the normotensive rats, moderate impairment of norepinephrine inactivation, however, was balanced by an appropriate reduction in central sympathetic discharge following sodium-loading. In the hypertensive rats, the peripheral disturbance in norepinephrine inactivation due to sodium-loading was obviously not balanced by an adequate withdrawal of central sympathetic discharge. The resultant hemodynamic change was a further increase in the sympathetically mediated vasoconstriction, which is regarded as at least one of the main mechanisms of the sodium-dependent acceleration of hypertension in SHRSP. (Hypertension 4: 773–781, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Inflatable suits were constructed for lower body compression in pigs and dogs. The suit for pigs encompassed hindquarters and part of the abdomen, and the smaller suit for dogs compressed only the hindquarters, leaving free the abdominal cavity. In conscious, diazepam-pretreated pigs, the compression lasted 30 minutes; during that period the blood pressure increased 50/38 mm Hg over the baseline. In chloralose-anesthetized dogs, the compression was extended to 3 hours; the blood pressure increase was 44/53 mm Hg. Blood pressure fell to the baseline immediately after decompression in both animals. In both species the substantial blood pressure increase was due to an increase of vascular resistance; this did not induce the expected baroreceptor-mediated bradycardia. In dogs, the blood pressure increase was accompanied by a large increase of plasma norepinephrine (from 179 to 975/). To test whether the increase of vascular resistance reflected the mechanical compression of the vessels under the suit, animals were pretreated with trimethaphan. In pigs the trimethaphan substantially decreased the vascular resistance and the blood pressure response. This indicated that a portion of the vasoconstriction occurred in areas outside the suit. Lower body compression is a new model to cause prolonged blood pressure elevation by noninvasive and nonpharmacologic means. The mechanism of the blood pressure elevation requires further investigation. (Hypertension 4: 782–788, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The effects of a moderate dietary salt restriction on intralymphocytic sodium content and pressor response to stress (mental arithmetic, handgrip, and bicycle exercise) were tested in 25 young subjects with borderline hypertension. The study was performed by a randomized, cross-over, within-patient, experimental design. Diet did not significantly reduce blood pressure at rest but did so significantly in both systolic and diastolic blood pressure during stress and exercise. Variations in diastolic blood pressure induced by stimulation correlated significantly with intralymphocytic sodium content both before and during low-salt diet whereas no correlation was found in the case of systolic blood pressure and heart rate variations. These findings suggest that in young subjects with borderline hypertension, sodium homeostasis and blood pressure regulation are somehow interrelated, and that a moderate dietary salt restriction reduces both intralymphocytic sodium content and pressor response to adrenergic stimulation. This could be useful in preventing the development of sustained hypertension. (Hypertension 4: 789–794, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Alterations in sodium countertransport and cotransport have been reported in red cells of patients with essential hypertension. We have investigated the relationship between these two systems by performing simultaneous measurements of the maximal rates of lithium-sodium (Li1-0) countertransport and outward sodium-potassium (Na-K) cotransport in red cells from normotensive and hypertensive subjects. Li1-Naocountertransport was assayed by measuring the Nao- Li efflux from cells loaded to contain 10 mmoles Li per liter of cells by incubation in isotonic LiCI. Na-K cotransport was assayed by measuring the furosemide-sensitive component of Na and K efflux into magnesium-sucrose medium from cells loaded by thep- sulfonic acid (PCMBS) procedure to obtain 50 mmoles of both ions per liter of cells. The mean values ( ± SE) for 16 normotensives and 22 hypertensives were (/cells × hour): Na countertransport = 0.29 ± 0.02 vs 0.51 ± 0.03 (p< 0.001); Na cotransport = 0.30 ± 0.03 vs 0.51 ± 0.05 (p< 0.005); and K cotransport = 0.34 ± 0.03 vs 0.60 ± 0.04 (p< 0.005). Li1-Na0countertransport correlated significantly with Na cotransport (r= 0.50,n= 38,p< 0.005) and K cotransport (r= 0.57,p< 0.005). This observation suggests that both transport systems are somehow regulated to be more active in this group of hypertensive patients. The increased cotransport in hypertensive patients is also apparent from two other measurements of Na and K fluxes in red cells suspended in Na medium. First, the furosemide-sensitive net Na efflux into Na medium was (mean ± SE) 0.25 ± 0.05 in 10 normotensive subjects and 0.50 ± 0.09 in 12 hypertensive patients. Second, the furosemide-sensitive net K efflux into Na medium was (mean ± SE) 0.25 ± 0.04 in 13 normotensive subjects and 0.43 ± 0.04 in 16 hypertensive patients (p< 0.005). We conclude that mean values for both Na countertransport and Na-K cotransport are significantly higher in the group of hypertensives than in the group of normal control subjects. (Hypertension 4: 795–804, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Previous investigations examining techniques to estimate sodium intake in free-living persons failed to consider a varying intake or were not conducted under circumstances in which the intake was actually known. To examine the utility of 24-hour and nocturnal urine collections as estimation of sodium intake under such conditions, we studied 43 white and black men and women ingesting a known sodium intake for 10 days that was randomly varied daily, with a mean intake of 150/+ 2SD (range, 50 to 250/). The mean 24-hour sodium excretion (UNaV) per day was 141/while the mean sodium intake was 151/. On a randomly selected day, both nocturnal and 24-hour UNaV estimated that day's sodium intake reasonably well (r= 0.55). A stepwise regression showed that including consideration of age and blood pressure improved the correlation (r= 0.70). However, to estimate mean sodium intake accurately for the entire 10 days, the average of several 24-hour collections was required. Nine collections were optimal (r= 0.75). Nocturnal specimens were not helpful; the average of all 10 collections correlated weakly (r= 0.30) with sodium intake. These data sugj.est that to estimate mean sodium intake accurately in free-living persons, only 24-hour collections are useful, although nocturnal collections arc helpful in evaluating compliance with low sodium intake. (Hypertension 4: 805–808, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

This study was designed to determine the roles of the sympathetic nervous system, adrenal medulla, and arginine vasopressin (AVP) in mediating pressor and plasma activity (PRA) responses to intraventricularly (ICV) administered prostaglandin E2(PGE2) in conscious rats. The ICV PGE2elevated blood pressure and caused increases in PRA, plasma AVP, and plasma norepinephrine and epinephrine. The pressor effect of ICV PGE2was not influenced by pretreatment with captopril, but was attenuated by the AVP antagonist, d(CH2)5Tyr(Me)AVP, and by phenoxybenzamine, and was completely abolished by the combination of the AVP antagonist and phenoxybenzamine. The PRA response to ICV PGE2was not affected by bilateral renal denervation or by phenoxybenzamine alone, but was attenuated by propranolol alone and was completely abolished by the combination of propranolol and phenoxybenzamine. Bilateral adrenomedullectomy did not affect the pressor response to ICV PGE2, whereas it attenuated the increase in PRA and completely abolished the increase in plasma epinephrine. These results suggest that the pressor effect of ICV PGE2is the result of increased sympathetic nervous system activity and is dependent on the stimulation of alphaadrenergic receptors and on AVP release. The pressor response to ICV PGE2is accompanied by but not dependent on an increase in PRA. The renin-stimulating effect of centrally administered PGE2is, at least in part, dependent on beta-adrenergic receptor stimulation by increased circulating catecholamines. (Hypertension 4: 809–816, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Sixteen untreated black patients with mild- to- hypertension and no evidence of target organ damage were matched for age, sex, casual blood pressure (BP), and socioeconomic status with 16 white hypertensives. All patients were studied under standardized conditions in the hospital where they underwent continuous intraarterial ambulatory monitoring of BP and assessment of BP control mechanisms. BP characteristics over prolonged periods of recording were similar for both groups, as were sinoaortic baroreflex activity and pressor response to isometric and dynamic exercise and to cold. Fasting cholesterol and triglyceride levels in both groups were similar. Resting plasma renin activity (PRA) was significantly lower in blacks, but no difference was observed in resting plasma norepinephrine levels. Urinary excretion of Na+and K+was also similar in both groups. Thus, results showed that casual BPs matched for black and whites, and recorded over a prolonged period, were similar in pattern, variability, and response to pressor stimuli. It appears that, if BP contributes to the different patterns of morbidity in blacks and whites, it is more likely to be the actual level of BP rather than differences in BP characteristics. (Hypertension 4: 817–820, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

SUMMARY Steady state levels of catecholamines (dopamine, norepinephrine, and epinephrine) were measured by the use of radioenzymatic techniques in discrete areas of the kidney (outer and inner cortex, outer and inner medulla) dissected by a “punch” technique from frozen kidney sections of salt-sensitive (DS) and salt-resistant (DR) Dahl rats fed a low or high salt diet. All three catecholamines were present in all areas of the kidney examined. There were gradients of concentrations of each catecholamine in different kidney areas. Renal medullary areas contained proportionally more dopamine than cortical areas. The proportion of epinephrine with respect to the total catecholamine content was relatively high in the inner medulla. Genetic factors and the amount of dietary salt influenced the catecholamine content in specific kidney areas, and these changes were different according to the area considered. DS rats when fed a high salt diet presented increased systolic blood pressure but no increased levels of dopamine in the inner medulla nor of norepinephrine in the outer medulla and outer cortex. Results suggest that either the uptake, release, storage, synthesis, or catabolism of kidney catecholamines is altered in Dahl salt-sensitive (DS) hypertensive rats and suggest specific roles for each catecholamine in discrete areas of the kidney. (Hypertension 4: 821–826, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID