摘要:

Electrical stimulation of fibers of passage through the fastigial nucleus increases arterial pressure. To identify nuclei that may project through the pressor region of the fastigial nucleus, we injected the retrograde tracer fast blue unilaterally at confirmed pressor sites in the nucleus. In seven rats, we found dense fluorescent labeling bilaterally in the external cuneate, lateral reticular, medial vestibular, and caudal prepositus hypoglossi nuclei, and contralaterally in the inferior olivary nucleus. There had been no reports of a cardiovascular role for the nucleus prepositus hypoglossi; thus, we sought to determine if electrical or chemical stimulation of that nucleus or the adjacent medial vestibular nucleus altered arterial pressure or heart rate in 24 anesthetized rats. Both types of stimuli to the caudal, but not the rostral, pole of the nucleus prepositus hypoglossi or to the medial vestibular nucleus elicited an increase in arterial pressure; bradycardia accompanied the former and tachycardia the latter. Both the nucleus prepositus hypoglossi and medial vestibular nucleus may participate in central cardiovascular regulation.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The objective of this study was to determine if ablation of the lateral parabrachial nucleus (LPBN) would prevent angiotensin II-induced hypertension in rats. Thirteen male Sprague- Dawley rats were studied. Bilateral electrolytic lesions in the LPBN were produced in six rats; the remaining seven rats were subjected to sham lesion surgery only. All rats were instrumented with vascular catheters and housed in metabolism cages. Daily measurements during the 16-day protocol included arterial pressure, heart rate, water intake, urine output, and urinary sodium excretion. Periodically throughout the protocol depressor responses to ganglion blockade and to blockade of V,-type vasopressin receptors also were measured. The protocol was divided into three control-period days, 10 days of continuous (24 hr/day) angiotensin II infusion (10 ng/min i.v.), and three recovery-period days. There were no significant differences between the two groups of rats for any variable during the control period. During angiotensin II infusion, sham-lesion rats exhibited a progressive increase in arterial pressure and the depressor response to ganglion blockade and a decrease in urinary sodium excretion. No other variable was significantly changed. In rats with LPBN lesions, arterial pressure was significantly increased only on days 1 and 3 of angiotensin II infusion. No other variable was affected. It was concluded that ablation of the LPBN in rats prevented sustained hypertension during intravenous infusion of angiotensin II by interfering with neurogenic pressor mechanisms normally activated by the peptide.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Vascular smooth muscle (VSM) transmembrane potentials (EM) were measured in situ in small branch arteries (150-300-μ;m o.d.), small branch veins (300-400-μ;m o.d.), arterioles (90- 150μm o.d.), and venules (80-250-μ o.d.) in the mesenteric and gracilis muscle and the arterioles and venules of cremaster muscle vascular beds in anesthetized rats with reduced renal mass hypertension (HT-RRM) and normotensive sham-operated RRM control rats. All rats were given a 4% NaCl diet for 2 weeks with water ad libitum. Relative to sham, HT-RRM mesenteric and gracilis arterial and venous vessels, but not the microvessels of the cremaster muscle bed, were less polarized during superfusion with normal physiological salt solution. Also relative to sham, hyperpolarization responses to local sympathetic neural (SNS) denervation with 6-hydroxydopamine were greater in mesenteric and gracilis small arteries, arterioles, veins, and venules but not in cremaster microvessels. The immediate (less than 5-minute) electrogenic depolarization response to local blockade of VSM Na+-K+ pump activity with 10−3M ouabain was similar between each respective HT-RRM and sham vessel pair in each vascular bed. These results suggest that in all three vascular beds: 1) significant SNS control of VSM Em(and active tone) exists all the way to the arterial and venous microvasculature (except cremaster venules); 2) in HT-RRM, such SNS control is elevated relative to sham in both arterial resistance and venous capacitance vessels in mesenteric and gracilis vascular beds but not in the cremaster microvessels; and 3) any circulating Na+-K+ pump inhibitors in the circulation of this volume-expanded model of hypertension do not appear to affect VSM tone in the vessels studied.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

It has been shown that endothelin-1 (ET-1) binding sites exist in the central nervous system and that the injection of intracerebroventricular ET-1 induces a pressor response. Therefore, we determined the neurohormonal and cardiovascular responses to intracerebroventricular ET-1 (25 pmol/kg) in conscious rabbits with chronically instrumented electrodes on the renal sympathetic nerve. Intracerebroventricular ET-1 provoked a prompt increase in arterial pressure and in renal sympathetic nerve activity within 5 minutes, and peak values were obtained at 20 and 40 minutes, respectively. Plasma epinephrine and norepinephrine reached peak values at 5-20 minutes. Plasma vasopressin and plasma glucose levels also increased significantly, but plasma osmolality, hematocrit, and serum sodium and potassium concentrations did not show any changes. Arterial blood gas analysis showed respiratory alkalosis. However, pretreatment with intravenous pentolinium (5 mg/kg), a ganglion blocking agent, abolished these neurohormonal and cardiovascular responses. Conversely, the same dose of intravenous ET-1 (25 pmol/kg) as that used in the intracerebroventricular experiment failed to cause any cardiovascular or renal sympathetic nerve responses. These results suggest that intracerebroventricular ET-1 acts in the central nervous system and causes a pressor response mainly through the enhancement of sympathoadrenal outflow.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

When Dahl salt-resistant (DR) rats are given mild post-deoxycorticosterone acetate (DOCA) hypertension, they will have, within 8 weeks, a 53% mortality on a high NaCl diet, without a rise of blood pressure. Forty-two DR rats were given DOCA in silicone (250 mg/kg) and 1% NaCl to drink. After 4 weeks, the DOCA and 1% saline were removed and replaced with a low NaCl diet and tap water. One week later, they were divided into two groups perfectly matched for blood pressure (154 mm Hg). One group had the aqueduct of Sylvius blocked with silicone and epoxy materials; the other group had a sham block. After 4 more recovery weeks on a low NaCl diet, blood pressure averaged 171 mm Hg in sham rats and 147 mm Hg in truly blocked rats (p<0.0001). Thus, the aqueduct block prevented most of the post-DOCA hypertension and permitted a strong post-DOCA recovery from the acute DOCA hypertension. The rats with the sham block had an actual rise in blood pressure during the post-DOCA recovery period. The vicious cycle leading to permanent post-DOCA NaCl hypertension was broken by the aqueduct block. Then both groups began an 8% high NaCl diet, and after 4 weeks, blood pressure averaged 184 mm Hg in sham and 155 mm Hg in truly blocked rats (p<0.0001). After 12 weeks on 8% NaCI, all sham rats had died (28 of 28), whereas only one of 14 truly blocked rats had died (93% reduction in mortality,/7 < 0.0001). The urinary albumin/creatinine ratio was 36 in sham rats versus only 14 in truly blocked rats (-62%,p<0.0001). The dry heart weights averaged 431 mg in the sham rats versus 310 mg in the truly blocked rats (-28%,p<0.05) even though the body weight of the sham rats averaged 6% less on the high NaCl diet In the post-DOCA NaCl period, it is likely that structural changes linger on in the third brain ventricle region, leading to post-DOCA hypertension and progression of renal lesions. An aqueduct block produces hydrocephalus of the third ventricle and thereby reverses the lingering post-DOCA structural effects, thus greatly reducing blood pressure, mortality rate, cardiac hypertrophy, and urinary albumin.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID