摘要:

SUMMARY Alterations in the dynamics of brain serotonin biosynthesis can lead to changes in cardiovascular function. It appears that the activation of cerebral serotonin receptors produces a pressor effect in normotensive rats but produces a depressor effect in nonnotensive cats or dogs. On the other hand, reductions in the levels of serotonin can prevent the onset of hypertension in some experimental hypertensive models and lower the blood pressure of organisms with established hypertension. The ability of brain serotonin to modulate arterial blood pressure may be mediated by the influences of the serotonergic neuronal systems on efferent sympathetic activity. Finally, the reduction in sympathetic outflow produced by increasing brain serotonin levels in dogs protects the heart against ventricular fibrillation and may, therefore, constitute a reasonable adjunct in the management of high-risk, cardiac-arrest patients.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Attempted correction of two-kidney, one clip Goldblatt hypertension in the rat was carried out by three techniques: removal of the constricting dip, removal of the Iscberaic kidney, and converting enzyme blockade by oral captopril. Since duration of hypertension is said to be a critical factor, groups of rats were studied after short term (< 6 weeks from clipping) and chronic (> 4 months) hypertension. Blood pressure, sodium balance, and plasma renin concentration (PRC) were followed before and after these correcting procedures. In a control group of animals, removal of a loose renal artery clip did not Influence blood pressure and only caused trivial postoperative retention of sodium. Undipptng, however, normalized blood pressure in both short-term and chronic hypertension. After a major postoperative fall, blood pressure returned to somewhat elevated levels after nephrectomy in animals with chronic (but not short-term) hypertension. Sodium balance became markedly positive with the fall in blood pressure of operated hypertensive anlmpu and was significantly correlated with the fall in blood pressure in these four groups at 7 days (r= 0.43). Captopril also produced a fall in blood pressure at 24 hours, with a positive sodium balance, although the relationship between blood pressure fall and sodium balance did not reach statistical significance (r= 0 JO). The PRC was elevated in all hypertensive groups, although individual values overlapped with values from normal rats and nonhypertensive rats with a loose renal artery dip. The PRC fell to normal or subnormal values after either operative procedure and stabilized for at least 2 months Independently of whether blood pressure fell or not. It is concluded that neither sodium retention nor renin hypersecretion maintains blood pressure In this model. Also, the rapidity of the blood pressure fall is not consistent with a role for vascular hypertrophy. Tbe greater efficacy of unclipping suggests that the revascularized kidney after this procedure exerts a vasodepressor function independent of sodium excretion or the renin-angiotensin system.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY In many experimental models, acute increases in sympathetic nerrous system activity produce disproportionately greater vasoconstriction in the renal vascular bed than occurs in most other vascular beds. Since increased sympathetic nervous system activity has been implicated in the patbogenesis of DOCA-salt hypertension in the rat, we hypothesized that an attenuation of renal sympathetic tone would delay the development of this form of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Hypertension-resistant (R) rats of the Dahl strain remain normotenslve on diets containing excessive sodium chloride, while hypertension-sensitive (S) rats rapidly become hypertensive when eating the same diet. In the present study, renal hemodynamlcs were investigated in Dahl rats eating normal or high salt chow for 4 weeks. The R rats eating sodium-enriched cbow were found to have significantly lower renal vascular resistance (RVR) than R rats on normal chow; RVR was identical in S rats on either diet. The reason for the failure of S kidneys to exhibit vasodilation during high salt ingestion was explored by examining renal vascular responses to interruption of the renal sympathetic nerves, renal sympathetic nerve stimulation (SNS), and to several vasoactive agents. Changes in RVR to nerve section and to SNS were similar in both strains regardless of diet Renal vascular responses to Intraarteritl norepinephrine were suppressed significantly by high salt intake only in the R rats. Changes in RVR to lntraarterlal angiotensin II were uniformly greater in S than in R rats, but were not altered by salt intake in either strain. Renal vasodilation in response to intraarterial acerylcholine was reduced in R rats on high salt intake, but was not affected by salt intake in S rats. It is concluded that S rats exhibit inappropriately high renal vascular tone during ingestion of excessive salt, and that this alteration is not the result of increased neurogenic activity or increased vascular reactivity to angiotensin II or norepinephrine.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Partial nephrectomy-salt hypertension (PN-SH) of the rat is associated with Na volume loading. As the hypertensive state evolves, the renomedullary interstitial cells (RIC) of the renal nubbin undergo major changes, decreasing significantly in number while the remaining ones exhibit degenerative changes. The antihypertenslve action of the RIC in the renal nubbin, as measured by transplants of fragmented papillae into hypertensive recipients, virtually disappears as the hypertension develops. The changes In the RIC occur whether vascular disease of the kidney is or is not overtly present. It is suggested that deficiency of the antihypertensive action of the RIC allows the prohypertensive effects of Na volume loading to operate without proper control. Thus, the sustained hypertensive state of this model does not appear to be due solely to volume expansion. Rather, It appears due to a combination of the effects of Na and volume and a renomedullary deficiency of hormonal type.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Over a 9-month period, the incidence and characteristics of hypertension followtng coronary artery bypass surgery were studied in a group of 52 patients. Hypertension occurred in 61% of the patients and was characterized by an increase in arterial blood pressure of 35 ± 2 mm Hg mean ± SEM during the early postoperative period. Preoperative blood pressures and hemodynamk variables were similar in those who developed hypertension and those who remained normotenshe. Ninety-four percent of those who developed hypertension as compared to only 40% of those who remained normotensive received propranolol during the 24 hours preceding surgery (x1= 15.4;p< 0.001). Maximal blood pressures during the first 5 hours following the termination of cardiopulmonary bypass were significantly positively correlated with preoperative propranolol dosage (p< 0.01). Hypertension was not associated with significant changes in plasma renin activity or angiotensin II levels, but concomitant plasma catecholamine concentrations were elevated significantly (p< 0.005). However, a similar rise in plasma catecholamine concentrations was found in those who remained normotensive. Hypertension was associated with an increase in systemic vascular resistance (p< 0.001) and left ventricular stroke work index [p< 0.05), and a fall in stroke volume (p< 0.005) and cardiac index (p< 0.001). These studies suggest that hypertension following coronary artery bypass surgery is common, results from an increase in systemic vascular resistance, is not renin-angiotensin mediated, and may, in part, be related to preoperative propranolol administration.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Male spontaneously hypertensive rats (SHR), 13 weeks old, received oral administration of captopril (SQ 14,225) daily at a dose of 10 mg/kg or 30 mg/kg; or water at 2 ml/kg, for 6 weeks. Captopril suppressed the development of hypertension slightly at the lower dose and completely at the higher dose. At 6 weeks of dosing, hemodynamlc parameters were measured by the tracer microspbere method and blood volume by the dilution method usingMCr erythrocytes. Cardiac output (CO) increased and mean blood pressure decreased in a dose-dependent manner; thus, total peripheral resistance decreased. Cerebral and renal blood flows increased in a dose-dependent manner while blood flow to other organs tended to increase or remained unchanged. There was no significant difference in the circulating blood volume among the three groups. In conclusion, long-term blockade of angiotensin converting enzyme (ACE) with captopril dilated blood vessels in the whole body, especially in the brain and kidney, and lowered blood pressure without causing plasma expansion or tachycardia.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Spontaneously hypertensive male rats (SHR) or normotenslve Kyoto-Wlstar (WKY) male rats underwent either sham or nerve growth factor antiserum (NGFAS) treatment during the first week of life. The NGFAS treatment prevented the development of hypertension in SHR bat did not prevent the development of left ventricular (LV) hypertrophy. At 48 weeks of age, various parameters of LV function were measured In the four treatment groups in vivo under general anesthesia. After the recording of resting parameters, homologous whole blood was transfused until the rise in cardiac output reached a plateau. At rest, LV systolic pressure of the NGFAS-treated SHR was significantly lower than that of the sham-treated SHR and not statistically different from that of the WKY rat. The LV end dlastolic pressures did not differ among the four groups. Both SHR groups had significantly lower cardiac, stroke, and contractility indices than did the WKY groups. Following vascular expansion, LV filling pressure, stroke index, and stroke work index rose in all groups. The response in the SHR was greater than that In WKY groups. Interestingly, the systolic pressure of the NGFAS- treated SHR rose to the same level as in the sham-treated SHR. Heart rate and calculated systemic vascular resistance fell following transfusion. The SHR appears to exhibit an altered response to increased filling pressure and increased afterload. Our findings are consistent with the concept of an alteration in the compliance of the LV in the SHR.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY Hypertension was induced experimentally by subjecting rats to vigorous shaking, 4 hours (at random) daily for 14 weeks. Systolic pressures measured with the tail-cuff method began to rise after the first week and were significantly derated on Weeks 3, 4, 6, 7, and 8, but reverted to normotensive levels thereafter despite continued shaking. A similar hypertension was then induced in another group of rats and when spontaneous remission occurred, pressor responsiveness was tested on the eleventh week by recording aortic pressures from indwelling catheters. Pressor responses to further shaking or electrical stimulation of the anterior hypothalamus were smaller in shaker-stressed than in control rats, while those to injected norepinephrlne were almost the same in both groups. Spike potentials recorded from postganglionlc sympathetic (splanchnic) nerves showed higher baselines but smaller increases in neural firing during hypothalamic stimulation in shaker-stressed than in control rats. These results suggest that while shaker stress alone can induce hypertension, the resulting blood pressure elevation is not sustained, perhaps because adaptation within the central nervous system concurrently reduces pressor responsiveness.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SUMMARY In an attempt to produce a form of chronic neorogenlc hypertension without the Increased blood pressure lability which b characteristic of total baroreceptor removal, selective aortic baroreceptor deafferentation (ABD) was performed In rats. Blood pressure, Mood pressure variability, heart rate, plasma and extracellular fluid volumes, and the effect of total autonomk blockade were determined in male rats 1 month following ABD. Rats with ABD had significantly higher systolic, diastollc, and mean arterial blood pressures than did sham-operated animals, but the standard deviation of pressure measured repetitively over a 1-hour period was not significantly greater. Total autonomk blockade with atroplne, propranolol, and pnentolamine lowered blood pressure and heart rate to a similar level In ABD and sham-operated rats. Extracellular fluid volume was not different In the two groups of rats, but plasma volume was significantly lower in rats with ABD. Despite the overall reduction in plasma volume, there was a significant positive correlation between plasma volume and blood pressure In ABD rats; no such correlation was observed in sham-operated rats. It was concluded that ABD produces a mild, chronic hypertension in rats without marked pressure lability. Although the hypertension appears to be "neurogenic" In that it is abolished by autonomic blockade, volume factors also may contribute to the increased blood pressure.

ISSN:0194-911X    

出版商:OVID    

年代:1980

数据来源: OVID