摘要:

The relationship between plasma levels of norepinephrine (NE) and sympathetic neural activity is discussed with special reference to human primary hypertension. Since sympathetic discharge is differentiated, neural activity to a given target organ will contribute variably to plasma NE levels in different situations. Hemodynamically, early primary hypertension is often characterized by a mild defense reaction-like pattern with signs of increased sympathetic activity to the heart and vasoconstriction in the renal and splanchnic vascular beds. Although important hemodynamically, these organs seem to be ofless importance as contributors to peripheral plasma NE levels. In contrast, muscle sympathetic activity and muscle vascular resistance is unchanged or reduced. Since this organ mass contributes importantly to plasma NE levels, especially in peripheral venous blood, it is not surprising that most patients with primary hypertension have normal NE levels. It is concluded that NE concentrations in forearm or mixed venous blood are unreliable indicators of sympathetic neural contributions to essential hypertension, tending to underestimate this element, and that regional measurements of NE overflow are needed for a reliable analysis.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The purpose of this review is to focus on alterations in vascular muscle membrane potentials (Em), ionic permeabilities, and ionic transport systems which may either contribute to or be a consequence of the hypertensive state. Three models of hypertension are discussed: 1) deoxycorticosterone- salt (DOCA-salt)-induced hypertension; 2) low-renin (presumably volume expanded) renal hypertension (LRRH); and 3) the spontaneously hypertensive rat (SHR) of the Okamoto-Aoki Kyoto- Wistar strain and its normotensive genetic control (WKY). The importance of studying all possible mechanisms of increased contraction in vascular smooth muscle is stressed.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The metabolism of inositol phospholipids of the erythrocyte membrane was compared in normotensive Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone SHR (SHR-SP) rats. This was performed on isolated ghost membranes by measuring the incorporation of32P from [γ−32P] adenosine triphosphate (ATP) into the diphosphoinositides (DPI) and the triphosphoinositides (TPI) which were the only32P-labeled phospholipids. 3JP-labeling of TPI was altered in adult and 3- week-old SHR as well as in SHR-SP compared to WKY controls; the radioactivity associated with TPI in hypertensive rats was about 30% lower than that associated with TPI in age-matched normotensive controls. By contrast, the radioactivity associated with DPI was similar in both hypertensive and normotensive rats. Measurement of the phosphoinositide distribution in both SHR and WKY indicates that the change observed in32P-TPI could not be accounted for by a reduced phosphatidylinositol content in SHR membrane. Measurement of the Mg2+-activated TPI-phosphomonoesterase and of the Ca2+-activated poly phosphoinosi tide phosphodiesterase activities did not show any significant difference between SHR and WKY. It thus appears that the altered phosphoinositide metabolism observed in hypertensive rats was a consequence of some alteration in the activity of kinases which are responsible for the conversion of phosphatidylinositol into DPI and TPI. These results also suggest that the defect in phosphoinositide metabolism observed in genetically hypertensive rats was not a consequence of the blood pressure elevation and could be related to the pathogenesis of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Previous studies have shown that a combination of avoidance conditioning schedules and increased intake of salt and water results in progressive hypertension in dogs within 14 days. The present experiments investigated the effects of increasing potassium intake upon blood pressure and heart rate of dogs made hypertensive by avoidance conditioning and salt-water loading. Two daily 30- minute sessions of free-operant avoidance conditioning were presented for 36 days during which isotonic saline was continuously infused into the arterial circulation (1.2 liters/day; 185 mEq Na+). Daily mean levels of systolic (22 ± 5 mm Hg) and diastolic (12 ± 4 mm Hg) pressure increased progressively in each dog during Days 1–14. Infusion of potassium chloride (100 mEq/day) from Days 15–28 resulted in progressive decreases in daily mean levels of systolic (−11 ± 2 mm Hg) and diastolic (−8 ± 1 mm Hg) pressure in each dog over this period. From Day 29–36, systolic (−8 ± 1 mm Hg) and diastolic (5 ± I mm Hg) pressure increased. Normotensive dogs not on the avoidance schedule showed no change in arterial pressure in response to 14 days of potassium chloride infusion. These experiments show that the level of potassium, as well as sodium, intake significantly determines blood pressure levels in this form of experimental hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Whether and to what extent sodium chloride infusions elevate blood pressure acutely were examined in conscious, normotensive, and spontaneously hypertensive (SHR) anephric rats. All animals were bilaterally nephrectomized 18 hours before study.Normotensive Wistar rats, allowed no food or water post nephrectomy (Groups I-IV), received either no infusion (Group I, control) or intravenous infusion of isotonic solutions of either NaCI, mannitol, or dextrose at a rate of 0.018 ml/min for 2 hours. Mean arterial pressure (MAP) measurements were determined directly by arterial catheter for control (C), 1 hour, and 2 hours. Blood pressure was increased above control in all groups at 1 hour and 2 hours (p< 0.05). The increase in MAP with NaCI was similar to that with no infusion or infusion of mannitol or dextrose. Normotensive Wistar rats (Groups V-VI) and SHR (Group VII) were allowed free access to food and water post nephrectomy and received either no infusion (Group V, control) or infusion of isotonic saline at a rate of 0.037 ml/min for 2 hours. MAP was elevated above control in all groups (V-VII) at 1 and 2 hours (p< 0.05). The magnitude of the rise was similar among all groups. Food and water accessibility post nephrectomy did not alter results. In both sets of experiments when saline was infused we were unable to identify any increase in blood pressure greater than control at either infusion rate. In fact, we continued the saline infusion in Group VI, until 100 ml of saline was infused without any elevation in blood pressure above control. We conclude that during the 2 hours of observations neither sodium nor chloride ions exert an independent eifect on MAP in normotensive or hypertensive anephric rats when compared to no infusion or isotonic isovolemic infusions of mannitol or dextrose during the same time period.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

We previously observed that the renal nerves facilitate sodium retention and contribute to the development of DOCA-salt hypertension in the rat. To determine whether the renal nerves also participate in the maintenance of DOCA-salt hypertension, we studied the effects of renal denervation after 3 or 10 weeks of DOCA-salt treatment on systolic blood pressure, urinary sodium excretion, creatinine clearance, and precapillary arteriolar wall/lumen ratios of renal, hindlimb muscle, and cremaster muscle vascular beds. Systolic blood pressures of animals given DOCA-salt reached a plateau by 3 weeks of treatment at which time a sham operation or renal denervation was performed. Sham operation in hypertensive animals resulted in no change in systolic blood pressure and no change in percent sodium intake excreted. Wall/lumen ratio of the renal precapillary arteriole in sham-operated hypertensive animals was increased compared to similar sized vessels in hindlimb and cremaster muscle. In contrast, renal denervation resulted in a natriuresis and an attenuation of the hypertension (208 ± 7 to 187 ± 7 mm Hg;p< 0.01). Wall/lumen ratio of the renal capillary arterioles in renal denervated animals was no different than similar sized vessels in hindlimb and cremaster muscle and significantly less than that seen in sham-operated animals (0.85 ± 0.05 vs 1.03 ± 0.06;p< 0.05). In another group of animals, sham operation or renal denervation was performed after 10 weeks of DOCA-salt treatment. At this time neither operation altered systolic blood pressure or sodium balance. In contrast to 3-week DOCA-salt-treated hypertensive sham-operated animals, renal precapillary arteriolar wall/lumen ratio of 10-week animals was no different than similar sized vessels in hindlimb and cremaster muscle. In addition, renal precapillary arteriolar wall/lumen ratio of 10- week DOCA-salt-treated renal-denervated animals was no different than that seen in 10-week DOCAsalt- treated sham-operated hypertensive animals. Creatinine clearance of the 10-week DOCA-salttreated sham-operated or renal-denervated animals was significantly (p< 0.01) lower than that of the 3-week DOCA-salt-treated groups (0.25 ± 0.14 vs 1.03 ± 0.10 ml/min). These data suggest that the renal nerves contribute to the early established phase of DOCA-salt hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. With time, the renal nerves play a diminishing role in the maintenance of established DOCA-salt hypertension in the rat, while other renal factors, including decreased glomerular filtration rate and probable fixed renal vascular changes, play an increasingly important role.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Most of the thallium uptake by canine iliac arteries (70%) was inhibited by ouabain. The component sensitive to ouabain was significantly increased by incubating tissues in K+-free solution and reduced by low temperatures, metabolic inhibitors, and loading with lithium. The apparent Km for thallium for the ouabain-sensitive uptake was 0.47 ± 0.046 inM. External K+inhibited thallium uptake and the apparent K1, was estimated to be 6.5 mM. Thallium thus appears to have a greater affinity for the ouabain-sensitive components. The residual component of thallium uptake was unaffected by maneuvers that affected the ouabain-sensitive uptake, which thus appears to be a suitable indicator of Na+pump activity in vascular smooth muscle.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

To determine if the effects of propranolol on hypertension and the arterial wal I persisted for a significant time after the medication was discontinued, various parameters were compared at 16 weeks in control turkeys (CC), in birds on the medication from 3 days to 16 weeks (PP), and in others that were treated only from 3 days to 10 weeks (PC). At 16 weeks, arterial blood pressure, maximum rate of pressure increase (dp/dt max), and aortic intimal hyperplasia were lowest in the PP group, intermediate in the PC birds, and highest in the CC turkeys. Likewise, the vascular wall constituted 61 % of the radius of the coronary arteries in the CC group, but only 52% and 45% in the PC and PP groups, respectively. At 16 weeks, heart rate was lowest and aortic tensile strength highest in the group that was treated for the entire period, at the end of which the average plasma propranolol level was 97 ng/ml. At the same age, heart rate and aortic tensile strength were approximately the same in the CC and PC groups, and propranolol was not detectable in the plasma. It is concluded that the administration of propranolol to hypertensive turkeys early in life reduced blood pressure, aortic intimal hyperplasia, and arterial wall thickness and that these effects persisted to a significant degree for at least 6 weeks after the medication was discontinued. The higher aortic tensile strength that was produced by propranolol did not persist.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The renal glomerulus converts arachidonic acid to vasoactive prostaglandins and thromboxanes. Since renal vascular resistance is increased in human and experimental hypertension, we have compared the synthesis of prostaglandins and thromboxane B2in isolated and superfused glomeruli from normotensive and spontaneously hypertensive rats (SHR). We used radioimmunoassay to measure prostaglandins E2, F2α, 6-keto-F1α(a metabolite of prostacyclin) and thromboxane B2(a metabolite of thromboxane A2). The relative abundance of these compounds was similar in normotensive and hypertensive rats, i.e., prostaglandin F2α> E2> thromboxane B2≃ 6-keto-F11α. In the presence of arachidonic acid, 6.6 μM, the glomeruli from hypertensive rats, aged 6 to 8 months, synthesized twofold more prostaglandin and thromboxane than the glomeruli from normotensive rats, whereas in the absence of added arachidonic acid, there were no significant differences between the prostaglandin synthetic capacity of the glomeruli. Glomerular prostaglandin degradation was not different in SHR compared to Wistar-Kyoto (WKY) rats. Increased glomerular synthesis of prostaglandins and thromboxane was also observed in glomeruli from 4- to 5-month-old SHR after stimulation of endogenous release of arachidonic acid in response to the calcium ionophore, A23187. Glomeruli from young SHR, aged 7 to 8 weeks, also showed enhanced production of prostaglandins and thromboxane despite small (20 mm Hg) differences of blood pressure. Prevention of the hypertension by captopril treatment, from the time of weaning, did not eliminate the differences of prostaglandin and thromboxane synthesis. We conclude that SHR glomeruli show a primary increase of prostaglandin and thromboxane synthesis. These increments are the result of increased cyclooxygenase activity and possibly augmented phospholipase activity. Thromboxane may partially account for the increased renal vascular resistance in SHR through direct vasoconstrictor action and prostaglandins may vasoconstrict indirectly through stimulation of renin release and formation of angiotensin.

ISSN:0194-911X    

出版商:OVID    

年代:1983

数据来源: OVID