ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The mortality of 3783 non-malignant hypertensive patients attending the Glasgow Blood Pressure Clinic between 1968 and 1983 and followed for an average of 6.5 years was compared with that in three control groups: the general population of Strathclyde a group of 15 422 subjects aged 45-64 years and screened in Renfrew and Paisley between 1972 and 1976, and a group of hypertensives seen in a blood pressure clinic based on general practice in Renfrew.Average blood pressure for men at entry to the Glasgow Clinic was 181/111 mmHg falling to 158/96 mmHg during treatment. Corresponding values for women were 185/109 mmHg and 161/96 mmHg. Seven hundred and fifty clinic patients (451 males) died during follow-up, the commonest causes of death in both sexes being myocardial infarction and stroke. All-cause age-adjusted mortality (deaths per 1000 patient-years) was 41.4 for men and 22.1 for women. At all ages in both sexes and for all levels of initial blood pressure mortality was less in patients whose blood pressure was reduced most. Without a randomized control group it is not certain that lower mortality in those with well controlled blood pressure was due to treatment, although this is the most likely explanation. Cigarette smoking, a history of myocardial infarction, angina or stroke, retinal arterio-venous nipping, raised blood urea, an abnormal electrocardiogram (ECG) and secondary hypertension were associated with increased risk, but heavy alcohol intake, obesity, haematocrit >45%, hypokalaemia and social class were not.Life table analysis showed that, despite some reduction of mortality by treatment, the relative risk to men and women in the clinic remained two- to five-times that of the general population. The benefits of treatment were not such as to restore normal expectation of life even when blood pressure was well controlled. Excess mortality in the clinic could not be explained by difference of smoking habit or social class. This suggests that there is in the hypertensive patients of the Glasgow Clinic an element of irreducible risk, that treatment may be beneficial in some respects but harmful in others, or that patients at particularly high risk are selectively referred to the clinic.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Sympatho-adrenal tone and reactivity were evaluated in anaesthetized normotensive and DOCA-salt hypertensive rats, by measuring arterial plasma concentrations of norepinephrine and epinephrine under basal conditions and following bilateral carotid occlusion. Baseline norepinephrine levels were significantly higher in DOCA-salt hypertensive animals than in their respective normotensive controls, whether they were studied with intact vagi or following bilateral vagotomy. The possibility of a relationship between the increased basal sympathetic fibres and the maintenance of DOCA-salt hypertension is strongly suggested by the finding of a significant correlation between mean arterial pressure (MAP) and basal circulating norepinephrine values in those animals. Furthermore, the epinephrine increase following carotid occlusion was found to be markedly potentiated in hypertensive animals (intact or vagotomized), suggesting adrenal medullary hyperreactivity to baroreflex activation in this model of hypertension. In normotensive rats the epinephrine increase induced by the carotid occlusion was greatly potentiated by the administration of an α2-antagonist (yohimbine), and completely abolished by administration of an α2-agonist (clonidine). In contrast, the epinephrine response to carotid occlusion, which is already enhanced in hypertensive animals, was unaffected by the same treatments. These results therefore suggest that adrenal medullary hyperreactivity observed in DOCA-salt hypertensive rats may be due to a dysfunction of an α2-adrenergic mechanism modulating adrenal medullary secretion.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The relationships between c0rdiac performance, coronary flow, coronary vascular resistance at maximal vasodilatation and myocardial oxygen consumption were determined in isolated hearts from spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY) and from SHR given metoprolol (β1-selective blocker) and felodipine (selective calcium antagonist) for 35 weeks. A working heart perfusion system was used. An oxygen electrode allowed continuous measurement of oxygen tension in the venous coronary effluentBlood pressure was reduced close to normal levels in treated SHR. Treatment also caused a substantial reduction of left ventricular weight.In both treated and untreated SHR, maximal cardiac performance, expressed as peak stroke volume, was enhanced above that of WKY at high perfusion pressures, while performance at low perfusion pressures was clearly reduced in the former groups. At a given workload, myocardial oxygen consumption (mmol 01/min per g) was reduced in both groups of SHR. This suggests a physiological structural adaptation to an elevated cardiac load in hypertension, where more myofibrils contribute to produce a given amount of work and therefore less oxygen is consumed per unit muscle mass. Coronary flow was reduced at any given perfusion pressure and oxygen extraction was increased in untreated SHR versus WKY. By causing regression of hypertensive structural vascular changes, treatment markedly increased coronary flow and correspondingly decreased oxygen extraction. Thus, by enhancing the myocardial nutritional supply with antihypertensive treatment, the reduced cardiac function at low perfusion pressure in untreated SHR was almost normalized.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Aggressive behaviour provokes a very high increase in plasma renin in aggressive male mice. We demonstrate that this occurs in mice with high as well as low concentrations of renin in the submaxillary glands, although the highest values were seen in the former. Plasma renin and angiotensinogen concentrations, as well as plasma renin activity, were measured before and after aggression. The theoretical plasma renin activity (generation rate of angiotensin I) was calculated from kinetic parameters and the renin and angiotensinogen concentrations. The Km|(Michaelis constant) was 3 µmol/l and the kcat(turnover number) was 0.15/s for the reaction between pure submaxillary mouse renin and mouse angiotensinogen. The measured plasma renin activity was much lower than that calculated from both the kinetics and the fall in angiotensinogen concentration. The decrease in angiotensinogen in vivo was independent of the renin concentration. Intraperitoneally injected renin mimicked the aggression-provoked renin increase and resulted in better agreement between measured and calculated parameters. This indicates, that during aggression, the mouse can inhibit and control the renin-angiotensinogen reaction.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

In anaesthetized cats reversible denervation of one kidney was performed by cooling of the left renal nerves to 3°C for 16 min. The response of the left (ipsilateral) kidney was compared with the response of the right (contralateral) kidney twice in the same animal: (1) when the right kidney was still innervated, and (2) after it had been surgically denervated. Left renal nerve cooling did not cause any changes in arterial pressure. In the left kidney, blood flow, vascular conductance, sodium and water excretions increased, and renin release decreased. Simultaneously in the contralateral kidney, no haemodynamic changes were observed, glomerular filtration was only transiently decreased, whereas sodium and water excretion significantly decreased and renin release increased. When left renal nerve cooling was repeated after surgical denervation of the right kidney, similar changes were observed in the left (ipsilateral) kidney, whereas all contralateral effects were abolished. These experiments suggest that tonically active afferent fibres from one kidney exert a reflex inhibitory action on sympathetic activity directed to the contralateral kidney controlling tubular sodium reabsorption and renin release.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The present study was designed to investigate in rats the influence of converting enzyme inhibition with captopril on blood pressure, plasma urea, plasma renin concentration (PRC), plasma aldosterone and plasma vasopressin, and to define the interrelationships between PRC and these variables during equal degrees of either hyponatraemic (furosemide, 40 mg/kg for 2 days) or hypernatraemic (48-h water deprivation) dehydration. Chronic treatment with captopril (40 mg/kg daily) decreased blood pressure by 19% in normally hydrated treated rats, by 27% in water-deprived treated rats and by 40% in furosemide-treated rats. Plasma renin concentration, plasma aldosterone and plasma vasopressin were increased during both hypo- and hypernatraemic dehydration. Captopril decreased plasma aldosterone in waterdeprived and furosemide-treated rats, whereas plasma vasopressin was unchanged. The significant correlation observed between plasma aldosterone and PRC in non-treated rats persisted in treated rats, the same level of plasma aldosterone being observed at values of PRC 10 times higher. On the other hand, the correlation between plasma vasopressin and PRC did not persist in captopril-treated rats. An increase in plasma urea was observed in both water-deprived treated rats and furosemide-treated rats. These data indicate that during hypo- and hypernatraemic dehydration, the renin-angiotensin system plays a role in regulating blood pressure, urea elimination and plasma aldosterone, but vasopressin regulation is not modified by its inhibition.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Previous studies have shown that 24-h urinary sodium (Na) excretion is similar in blacks and in whites. However, a significantly lower potassium (K) excretion by blacks, with a consequent rise in the Na:K excretion ratio, has been observed. Faecal electrolyte excretion has not been measured. Ten normotensive blacks and 11 normotensive whites on a free diet were studied. Simultaneous 48-h urine and faecal collections were made. The results of the urinary measurements were in accordance with those of previous studies, in that 24-h urinary K excretion by blacks (38.2 ± 12.4 mmol) was significantly lower than that of whites (78.3 ± 16.6 mmol). As a result, there was a significantly higher urinary Na:K ratio in the black group. The mean 24-h faecal K excretion of the black group (15 ± 7.3 mmol) was not significantly lower, even when corrected for weight, than that of the white group (20.8 ± 10.8 mmol). It is concluded that the low urinary K excretion of South African urban blacks, compared with whites, is a reflection of a lower dietary K intake.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The interacting effects of potassium with the dopaminergic control of mineralocorticoid release were evaluated in normal man. Sixteen male healthy volunteers [27 ± 6 (s.d.) years] on a 200 mmol sodium (Na+) and 60 mmol potassium (K+) diet (control) received a K+load of 200 mmol/day for 6 days (high-K+diet). Basal plasma aldosterone and 18-OH-corticosterone (18-OH-B) levels were significantly increased after 6 days of the high-K+diet, whereas basal levels of 18-OH-deoxycorticosterone (18-OH-DOC) and corticosterone remained unchanged. Fifteen minutes after 10 mg i.v. of the dopaminergic antagonist, metocloprarnide, a significant increase was only obtained for basal plasma aldosterone and 18-OH-B levels. The absolute rise of aldosterone and 18-OH-B induced by metoclopramide was greater (P < 0.01) after K+supplementation. However, the relative increase of these hormones was similar before and after K+loading. Basal plasma renin activity increased significantly under high-K+diet.The results indicate that K+homeostasis must be taken into account when estimating absolute response of aldosterone and 18-OH-B to dopaminergic antagonism.

ISSN:0263-6352    

出版商:OVID    

年代:1986

数据来源: OVID