摘要:

To determine whether vascular smooth muscle cells around intestinal arterioles of various sizes undergo comparable changes in spontaneously hypertensive rats, 4- to 6-week-oId (n = 10) and 17- to 19-week-old (n = 10) rats from the Wistar-Kyoto and the spontaneously hypertensive strains were used to study the external morphology of vascular smooth muscle cells by scanning electron microscopy and the vessel wall cross-sectional characteristics by light microscopy. At the tune of fixation all vascular tone had been abolished. Scanning electron microscopy analysis revealed that all Wistar-Kyoto and spontaneously hypertensive rats at a given age have spindle-shaped vascular smooth muscle cells of comparable length and longitudinal width for a given branching order of arterioles. However, normal maturation is associated with elongation and widening of the vascular smooth muscle cells. Light and sinning electron microscopy indicated that a monolayer of vascular smooth muscle cells, wrapped at almost 0 degrees to the vessel's radial axis, is maintained in adult spontaneously hypertensive rats. The radial thickness of this vascular smooth muscle cell monolayer was significantly (p < 0.025) increased for only the largest arterioles of young and adult spontaneously hypertensive rats. This radial thickening of individual vascular smooth muscle cells increased the muscular component of the wall area for the largest arterioles by about 50% in adult spontaneously hypertensive rats. Other smaller submucosal arterioles of young and adult spontaneously hypertensive rats had normal vessel wall and vascular smooth muscle cell characteristics. These data indicate that hypertrophy in the smooth muscle cell's radial dimension is the primary morphological change in intestinal arterioles of spontaneously hypertensive rats. However, the vascular smooth muscle cell hypertrophy is confined to the largest arterioles such that the remaining smaller arteriolar vessels in the spontaneously hypertensive rat retain a normal smooth muscle cell and overall wall morphology.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

In normotensive Sprague-Dawley rats stimulation of renal mechanoreceptors and chemoreceptors by increasing ureteral pressure and retrograde oreteropelvic perfusion with 0.9 M NaCJ results in a contralateral inhibitory renorenal reflex response with contralateral diuresis and natriuresis. Since efferent renal nerve activity is increased in spontaneously hypertensive rats (SHR) and renal denervation delays the onset of hypertension in SHR in association with increased diuresis and natriuresis, the present study was undertaken to examine whether renorenal reflexes were altered in SHR compared with normotensive Wlstar-Kyoto rats (WKY). In WKY mean arterial pressure was 113 ± 2 mm Hg and remained unchanged during renal mechanoreceptor and chemoreceptor stimulation. Increasing ureteral pressure 35 mm Hg increased Ipsilateral afferent renal nerve activity 4.5 ± 1.7 resets/min, decreased contralateral efferent renal nerve activity 3.2 ± 0.8 resets/min, and increased contralateral urine flow rate 33 ±4% and urinary sodium excretion 49 ± 8%. Similarly, retrograde ureteropelvic perfusion with 0.9 M NaCl increased ipsilateral afferent renal nerve activity 2.5 ± 0.6 resets/min, decreased contralateral efferent renal nerve activity 2.4 ± 1.1 resets/min, and increased contralateral urine flow rate 39 ± 5% and urinary sodium excretion 38 ± 8%. Stimulating renal mechanoreceptors and chemoreceptors to the same extent in SHR failed to increase ipsilateral afferent renal nerve activity, decrease contralateral efferent renal nerve activity, and produce a contralateral diuresis and natriuresis. It is concluded that renorenal reflexes are impaired in SHR. Failure of Ipsilateral afferent renal nerve activity to increase during renal mechanoreceptor and chemoreceptor stimulation indicates a peripheral defect at the level of the renal sensory receptors. This abnormality in the renorenal reflex control of renal function may contribute to hypertension in SHR by promoting excess sodium and water retention.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The possible role of catecholamlnes in the abnormal renal response to salt loading, a genetic defect resulting in hypertension in the salt-sensitive strain of Dahl rats, was investigated by measuring the adrenal synthesis of norepinephrine, epinephrine, and dopamine as well as their content In several tissues and the urinary excretion of these catecholamines as well as some of their metabolites at the height of salt-induced hypertension. We found that salt-sensitive Dahl rats, compared with salt-resistant Dahl rats, have a higher adrenal synthesis of [3H]norepinephrine following a pulse injection of [3H]tyrosine, a higher adrenal norepinephrine and epinephrine content but a lower kidney and heart ventricle content of dopamine and norepinephrine, and a decreased excretion of urinary dopamine, dihydroxyphenylacetk acid, 3-methoxytyramine, and homovanillie acid. These data suggest that the primary abnormality in salt-sensitive Dahl rats may be their inability to turn off, during high salt intake, then* increased adrenal norepinephrine synthesis from dopamine. The abnormal catecholamine response of salt-sensitive Dahl rats to high salt intake indirectly suggests increased noradrenergk activity and decreased dopaminergic activity in the kidney, which may be important mechanisms in the sodium retention and hypertension of these rats.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We tested the hypothesis that the antihypertensive effects of dietary taurine supplementation in deoxycorticosterone acetate (DOCA)-salt rats may be attributed to the suppression of sympathetic nervous system activity. In uninephrectomized rats treated with DOCA while receiving 1 % NaCl solution for 2 weeks, systolic blood pressure was significantly increased as compared with that in control rats treated with vehicle suspension and tap water. Sympathetic nervous system activity was assessed by tissue norepinephrine turnover, which was determined from the rate of decline of tissue norepinephrine concentration after the administration of α-methyl-p-tyrosine, a potent inhibitor of the rate-limiting step of catecholamine synthesis. Cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure (4°C, 8 hours) were markedly increased in DOCAsalt rats as compared with controi rats. Also, DOCA-salt rats had increased depressor response to hexamethoniom bromide, a ganglion blocker. In contrast, supplementation of 1 % taurine in DOCAsalt rats attenuated the development of the hypertension associated with the normalization of both the Increased depressor response to ganglionic blockade and the accelerated cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure. Taurine supplementation in control rats, however, had no effect on blood pressure or norepinephrine turnover during cold exposure. These results suggest that taurine supplementation suppresses sympathetic overactivity in DOCA-salt rats, thus leading to inhibition of the development of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Conscious two-kidney, one clip rats with 150 mm Hg or higher systolic blood pressure were infused with saralasin for 60 minutes. Those with a blood pressure decline of 30 mm Hg or more were classified as saralasin-sensitive; those with a decrease of 10 mm Hg or less were considered saralasin-resistant. The animals were then housed in metabolic cages. Groups of sham-operated normotensive, saralasin-sensitive or saralasin-resistant two-kidney, one clip (2K1C) rats were infused with atrial natriuretic factor (Arg 101-Tyr 126), 100 ng/hr per rat, for 6 days. Corresponding control groups were sham-infused. Blood pressure was initially higher in the saralasin-sensitive groups (176 ± 6 and 181 ± 1 mm Hg, respectively) than in the saralasin-resistant groups (160 ± 4 and 169 ± 4 mm Hg, respectively). Atrial natriuretic factor infusion produced a gradual decline in blood pressure to 128 ± 5 mm Hg, but only in saralasin-sensitive 2K1C animals. Urinary volume, initially higher in saralasin-sensitive hypertensive than in normotensive rats, was depressed during atrial natriuretic factor infusion. Urinary sodium excretion and water intake showed the same tendency, but the changes were not significant. No such modifications were observed in saralasin-resistant or shamoperated rats infused with atrial natriuretic factor. Body weight, which was higher in normotensive animals, was unchanged during atrial natriuretic factor infusion. Saralasin-sensitive, noninfused 2K1C rats were the only group with higher plasma renin activity than sham-operated, normotensive controls. Plasma aldosterone was higher in the former than in the other five groups. Saralasinresistant 2K1C rats, infused or not, or sham-operated rats infused with atrial natriuretic factor, had plasma aldosterone levels no different from those of normotensive controls. A positive correlation was noted between plasma renin activity and plasma aldosterone (r = 0.64,p< 0.001). The atrial content and concentration of immunoreactive atrial natriuretic factor were similar in all groups. These results suggest that the hypotensive response observed in saralasin-sensitive 2K1C rats during chronic atrial natriuretic factor infusion could be secondary to an inhibitory effect on renin release and that a decrease in the latter could play a role in the depression of plasma aldosterone.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Plasma phosphate values are significantly lower in spontaneously hypertensive rats (SHR) than in normotensive Wistar-Kyoto rats (WKY). In this study, we increased plasma phosphate in SHR by a high dietary phosphate intake and followed the effects on blood pressure. Fifteen male WKY and 15 male SHR were housed from 4 weeks of age up to 26 weeks. At 4 weeks of age all SHR manifested a hypophosphatemia compared with age-matched WKY (F = 62,p< 0.0003). At 5 weeks of age, the rats were divided into three diet groups: a control group, a group receiving 1.41% (wt/vol) KCI in drinking water, and a group receiving 2% (wt/vol) K2HPO4 KH2PO4 in drinking water. In the control (F = 16.2,p< 0.02) and KCI groups, (F = 36.3,p< 0.03), hypophosphatemia persisted throughout the study. The phosphate-supplemented diet normalized plasma phosphate level in SHR but did not change plasma phosphate level in WKY. As a consequence, no difference in plasma phosphate level between WKY and SHR was present in the group receiving additional phosphate from that time on (F = 1.2, p>0.41). The phosphate-supplemented diet significantly decreased systolic blood pressure in both strains. In phosphate-supplemented SHR, a significant decline in systolic blood pressure was observed from 20 weeks of age on (at 20 weeks of age: 222 ± 3 mm Hg for control SHR vs 198 ± 5 nun Hg for phosphate-supplemented SHR;p< 0.0003). In phosphate-supplemented WKY, a slight but significant decrease hi systolic blood pressure was observed from 24 weeks of age on (at 25 weeks of age: 133 ± 1 mm Hg for control WKY vs 125 ± 1 mm Hg for phosphate-supplemented WKY;p< 0.0004). The KCI diet had no significant effect on systolic blood pressure in either strain. Plasma electrolyte (sodium, potassium, calcium, and magnesium) levels were not influenced by the two diets throughout the study. We conclude that a high dietary phosphate intake, with concomitant normalization of hypophosphatemia, results in a decrease in blood pressure in SHR. The phosphate-induced hypotensive effect was not apparent until 15 weeks after initiation of the diet. The mechanism behind this effect remains to be elucidated.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The gene for atrial natriuretic factor is expressed within the adventitial cells of the rat aortic arch. Atrial natriuretic factor transcripts, similar in overall size (1100–1200 nucleotides) and 5-termini to those found in the atria, were identified in the arch. Much lower levels (−10–20%) of these transcripts were present in distal thoracic aorta. Atrial natriuretic factor peptide was localized by immunocytochemlstry to the adventitia of the arch in regions thought to harbor the aortic baroreceptors. These data suggest a previously unsuspected role for the peptide in regulating systemic blood pressure through the baroreceptor reflex.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID