ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

To examine tbe role of rasopressin (VP) in DOCAhyphensalt hypertension, arterial pressure and renal vascular reactirity were studied in control Longhyphenerans (LE) rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). Vascular reactirity to norepinephrine, VP and angiotensin II was assessed in isolated kidneys perfused at constant flow. LE rats snowed an increase in arterial pressure (AP) which was significant at 2 weeks post DOCA and averaged 180 mm Hg at 4 weeks. DI rats lacking VP showed no rise in AP after DOCA; however, DI rats given VP and DOCA developed hypertension with a course and magnitude similar to that observed in LE rats. At 6 to 10 weeks post DOCA, renal vascular reactivity to all agents was increased in LE rats and DI rats replaced with VP. Nonnotensive DI rats lacking VP snowed depressed reactivity. Assessment of changes in reactirity at 3 days post DOCA showed that changes preceded tbe rise in AP. These data suggest that VP may play a primary role in the patbogenesis of DOCA hypertension and that its mechanism may involve an induction of increased vascular reactirity. (Hypertension 4: 3–12, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Vascular responsiveness to nitroprusside and to norepinephrine was examined in two different preparations from DOCA hypertensive and normotensire control Spraguehyphendawley rats. The bloodhyphenperfused renal vascuiatures of DOCA hypertensive rats were significantly more sensitive than those of normotensiTe controls to the vasodilator action of low doses of nitroprusside. At high doses, responses in DOCA hypertensive and normotensive rats were similar. Since basal “structural” vascular resistances were greater in the hypertensive rats, it is possible that further vasodilation with nitroprusside was impeded more in DOCAtreated than in control rats. Nitroprusside produced a greater degree of vascular smooth muscle relaxation in tail artery strips from DOCA hypertensive rats than in those from normotensive controls. The current study is the first characterization of the effects of a vasodilator in mlneralocortlcoM hypertension. The two preparations gave divergent results with respect to vascular sensitivity to norepinephrine. When compared with control rats, the DOCA hypertensive rats showed a greater sensitivity to norepinephrine in tail arteries but a lesser renal vascular reactivity. It is evident that one must take a number of variables into consideration when characterizing changes in vascular responses that occur in a given model of hypertension: 1) the region of the vasculature (renal vs caudal artery); 2) the level of the arterial tree (conduit vs resistance vessels); 3) the technique employed for measurement of vascular changes (smooth muscle contraction vs vascular resistance changes); 4) the initial vasoconstrictor tone of the preparation; and 5) the agonist used (nitroprusside vs norepinephrine). (Hypertension 4: 13–19, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Prerious evidence shows that salthyphensensitive (S) rats have a net increase in plasma mlneralocorticoid activity due to l & -hydroxyhyphenll-deoxycorticosterone and decreased urinary kallikrein excretion compared to salthyphenresistant (R) rats. Since minermlocorticolds stimulate urinary kallikrein excretion, these results are inconsistent. This inconsistency was explained by the fact that, while R rats responded normally to treatment with deoxycorticosterone (DOC) by an Increase in urinary kallikrein excretion, S rats showed no change in urinary kallikrein even when treated with 10 mg of DOC/day for 24 days. S and R rats responded identically to DOC with changes in muscle electrolytes and relative hypertrophy of the renal distal tubule. Other measures of chronic mlneralocorticoid response in S rats beside kallikrein were, therefore, intact. It was found that S rats were capable of responding to Na deficient diet with an increase in urinary kallikrein comparable to R rats. It was argued, therefore, that mineralcocorticoid receptor mechanisms and distalhyphentubular cell responsiveness are intact in S rats. Mild glomerular and tubular scarring was found in S rats and the severity of renal lesions was increased by DOC treatment in S rats. These lesions correlated well with blood pressure and protelnuria. No such lesions were present in control or DOC treated R rats. It was suggested that failure of urinary kallikrein to respond to DOC in S rats may be a secondary phenomenon resulting from renal damage. (Hypertension 4: 20–26, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Segments of carotid and tall artery, and thoracic aorta from control and hypertensive animals (DOCA + salt) were used for the study of mechanics and/or chemical composition. Pressurehyphendiameter measurements were made on intact segments under conditions of actire (145 mMhyphenK+) and passive (Ohyphenca++and 2 mMhyphenEGTA) smooth muscle. Segments were used for chemical analyses of connective tissue content, water spaces, and electrolyte content. The passive stiffness of carotid and tail arteries increased monotonically with time. The carotids showed significant changes after two weeks of hypertension while the tail arteries only after 12 weeks. The collagen and total connective tissue content of the hypertensive arteries was decreased while collagen/elastln was unchanged. Smooth muscle activation produced larger changes in diameter of hypertensive arteries especially at higher values of transmural pressure. Maximum active force development was increased in carotid arteries at each time period from +2 weeks on while it was Increased for the tall arteries only at +2 and +4 weeks. Relative cellular volume of these arteries was monotonically increased with hypertension. Maximum active force normalized to cellular content was not significantly different for carotid arteries from control and DOCA rats. For hypertensive tall arteries normalized on this basis force development remained elevated at +4 weeks but was significantly reduced at +12 weeks. Not all of the responses to smooth muscle activation are monotonic with duration of hypertension, nor can all of these changes be explained on the basis of changes in cellular volume. (Hypertension 4: 27–38, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Arterial barereflex control of heart rate is impaired in young men with borderline or mild hypertension. Despite this impairment, these subjects often hare exaggerated increases in rascular resistance during orthostatk stress. We considered the possibility that this exaggerated reflex vasoconstriction might reflect augmented cardiopulmonary baroreflex control of vascular resistance m borderline hypertension (BHT). Accordingly, we studied cardiopulmonary baroreflex control of forearm rascular resistance in nine BHT men with blood pressure intermittently above 150/90 mm Hg and in seven nonnotensive (NT) men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP −5 to −2 0 mm Hg), which decreases cardiac filling pressures. Baseline mean arterial pressure was 99 ± 3 mm Hg (mean ± SE) in BHT vs 83 ± 2 mm Hg in NT (p< 0.05). Baseline forearm resistance was also higher in BHT than in NT: 19 ± 2 vs 13 ± 1 mm Hg/ml/mln/100 ml or units (p< 0.05). Reflex increases in forearm resistance during LBNP were greater (p< 0.05) in BHT than in NT (8.6 ± 1.7 vs 4.5 ± 1.1 units during LBNP −20). Increases in arterial pressure and forearm resistance during a cold pressor test were not significantly different in the two groups. Thus, the augmented response to LBNP could not be attributed to a nonspecific influence of increased baseline resistance or a generalized abnormality in reflex control. In summary, the results of this study suggest that there is augmentation of the tonic inhibitory influence of cardiopulmonary baroreceptors in humans with BHT. (Hypertension 4: 39–46, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

We used the neck chamber technique to study carotid baroreceptor control of blood pressure in 18 renovascular hypertensive subjects. Carotid baroreceptor*were stimulated or deactivated for 2 minutes by applying graded reductions or increases in the neck tissue pressure (NTP) outside the carotid sinuses. The sensitivity of the baroreflex was separately calculated for these two conditions by the coefficients of the linear regressions relating the changes in NTP to the resulting changes in mean arterial pressure (MAP, catheter measurement). Baroreceptor deactivation increased MAP, and the sensitivity of the baroreflex was 0.12 ± 0.07 in an early (5 to 15 seconds) and 0.32 ± 0.05 in a late (90 to 120 seconds) phase of the stimulus application. Baroreceptor stimulation reduced MAP, and the baroreflex sensitivity was in this instance 0.66 ± 0.08 and 0.50 ± 0.08 respectively. Both these sensitivities were significantly greater than those obtained for the baroreceptor deactivation. These responses entirely reproduced those of essential hypertensive subjects, but differed from those of norraotensive subjects in whom baroreflex sensitivity was greater for carotid baroreceptor deactivation than for stimulation. Our findings indicate that carotid baroreceptor control of blood pressure undergoes a marked resetting in renovascular hypertension. The similarity of the baroreflex between renovascular and essential hypertension suggests a secondary origin of the resetting La man. (Hypertension 4: 47–50, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Glomerular bemodynamics were studied by mJcropuncture technique in the undipped kidney in rats in which modest two kidney Goldblatt hypertension was maintained for 4 weeks and in normotensive controls. Both groups ingested less than 2 mEq Na+/day. In hypertensive rats at micropuncture, mean hydrostatic pressure was elevated both systemically (128 ± 5 vs 113 ± 3 mm Hg, p < 0.05) and within glomerular capillaries (55 ± 2 vs 48 ± 1 mm Hg, p < 0.05), resulting in an Increase in the transglomerular hydrostatic pressure gradient (40 ± 2 TS 33 ± 1 mm Hg, p < 0.05). The glomerular capillary permeability coefficient, however, was decreased in the hypertensive rats (0.063 ± 0.017 vs 0.115 ± 0.011 nl/s/g kw/mm Hg, p < 0.05), resulting in no change in nephron filtration rate (38.9 ± 2.3 TS 39.9 ± 2.5 nl/min/g kw). Nephron plasma flow also remained unchanged (154 ± 10 vs 140 ± 7 ml/mln/g kw). In separate studies in this model of hypertension, saralasin infusion demonstrated a peripheral effect of circulating angiotensin II which was increased over controls. Kidney mass and GFR were not different between clipped and undipped kidneys. No consistent abnormalities were observed by light or electron microscopy either in glomeruli or in vessels in the undipped kidney. This study demonstrates that glomerular bemodynamics may be altered early In the course of modest hypertension in this model without altering blood flow or fUtration rate. The deaease in glomerular capillary area and/or permeability (LpA) in the hypertensive rats could be either a result of the increased effect of circulating angiotensin II or the direct effect of glomerular capillary hypertension. (Hypertension 4: 51–57, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Clearance and micropunctnre experiments were performed to eraluate the influence of converting enzyme inhibition (CEI) (SQ 14,225) on renal hemodynamics, glomerular filtration rate (GFR), segmental vascular resistances, and superficial nephron function in anesthetized sodium restricted dogs. In one series (n = 8), renal blood flow (RBF) and GFR exhibited a high degree of autoregulatory efficiency when renal arterial pressure (RAP) was reduced from 126 ± 5 to 86 ± 1 mm Hg. With RAP maintained at the reduced level, CEI elicited increases in RBF (3.9 ± 0.3 to 5.8 ± 0.5 ml/min per g kw) and GFR (0.81 ± 0.03 to 0.94 ± 0.04 ml/min per g kw). With return of RAP to spontaneous levels during continued CEI, RBF and GFR autoregulatory efficiency was maintained, and was similar to that observed in control dogs subjected to the same procedures (n = 5). In the micropuncture experiments (n = 12), RAP was maintained at the reduced level (87.5 ± 87.9 mm Hg), and measurements were made before and during CEI. Proximal tubule pressure, peritubular capillary pressure, stop flow pressure, and single nephron GFR (SNGFR) increased significantly. Regression analysis suggested that the increases in SNGFR were associated with small increases in the filtration coefficient. CEI reduced preglomerular resistance by 29% to 35% and efferent arteriolar resistance by 24% to 32%. These results Indicate that the increased activity of the renin-angiotensin system that occurs during salt restriction exerts approximately equivalent vasoconstrictor influences on both preglomerular and postglomerular vascular resistance elements. (Hypertension 4: 58–68, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Conscious rats with twohyphenkidney one dip Goldblatt hypertension had the constricting dip removed during continuous infusion of either dextrose, saralasin, or captopril. Other dextrosehypheninfused animals underwent removal of the ischemic kidney or a sham procedure. Direct arterial blood pressure (BP) was recorded throughout the 15-hour preoperative and subsequent 24-hour postoperative period. Rats were studied in the “early” phase (1–3 weeks duration) or “chronic” phase (> 4 months) of hypertension. Animals subjected to a sham procedure returned to preoperative BP values. The BP of animals undipped or nephrectomlzed did not return to previous hypertensive levels. Instead, a biphasic response was seen where BP partially recovered from an operative fall and then slowly declined to normal at 24 hours; this effect occurred in both stages of hypertension. At 24 hours, removal of the ischeraic kidney was as effective as removal of the constricting dip in the correction of both eariy and chronic phase hypertension. Rats infused with saralasin or captopril demonstrated an acute (within 2 hours) and sustained fall in BP, but not to nonnotensive levels. This fall was significant In all animals (p< 0.01) apart from chronic phase rats infused with saralasin where no significant fall was seen. Although animals infused with saralasin or captopril commenced at a lower preoperative BP, the biphasic pattern of response to undipping was identical to that of dextrosehypheninfused undipped rats. Thus, sustained inhibition of the reninhyphenangiotensin system did not modify the correction of hypertension produced by removal of the constricting clip, and the response to surgical correction did not appear to be entirely mediated by changes in the activity of the reninhyphenangiotensin system, particularly in the chronic stage. Equally, the rapidity of correction is not consistent with a role for vascular hypertrophy. (Hypertension 4: 69–76, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID