摘要:

Arterial and venous compliances are decreased in men with sustained essential hypertension. The reduced arterial compliance acts to maintain systolic pressure and end-systolic stress, thus contributing to the development of cardiac hypertrophy. Since cardiac output remains within the normal range in the hypertrophied hypertensive heart, elevated left ventricular pressures, and therefore increased cardiac filling pressures, are necessary if an adequate stroke volume is to be maintained. In hypertensive persons, reduced venous compliance acts to maintain the filling pressure of the heart in the presence of reduced intravascular volume. In patients with hypertension, even if compliance changes have been initiated by the elevated blood pressure itself, the reduced arterial and venous compliance observed in cross-sectional studies is not simply the mechanical consequence of the elevated blood pressure, but also reflects intrinsic alterations of the vascular wall. Consequently, blood pressure reduction caused by antihypertensive agents is not constantly associated with a reversion of the decreased vascular compliance. Such observations may be of importance in the consideration of cardiovascular morbidity and mortality in patients treated for hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Characterization of the renal effects of calcium entry blockers has not been easy because the inhibition of Ca2+cellular influx alters several regulatory functions. The ability of calcium blockers to dilate renal vasculature and to increase glomerular filtration rate is largely determined by the preexisting vascular tone. However, the increments in sodium excretion could occur without alterations in renal hemodynamics. Calcium blockers could increase sodium excretion by inducing a redistribution of renal blood flow toward juxtamedullary nephrons, by inhibiting tubuloglomerular feedback responses, or by a direct action on the tubular transport of sodium. These effects are poorly understood at present. In vitro studies show that the blockade of calcium entry enhances renin secretion and decreases prostaglandin synthesis. This dissociation has not been found during longterm administration, which has been proved to be effective for the treatment of essential hypertension with normal maintenance of renal function. In this respect, there are reports indicating that calcium blockers are particularly effective in a subgroup of patients with essential hypertension who exhibit subtle but detectable alterations in calcium metabolism. Further studies are needed to determine whether this significant response to calcium blockers is due to correction of an early defect of calcium cellular kinetics that initiated the increase in blood pressure.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We examined the relationship of intraocular pressure and the development of onekidney, one wrapped (perinephritic) hypertension in the dog. Conscious femoral arterial pressure (direct arterial puncture) and intraocular pressure (Schiotz tonometer) were measured weekly before and after the surgical induction of hypertension in 11 healthy male mongrel dogs and before and after unilateral nephrectomy in 15 normotensive control dogs. Preoperative mean arterial pressure (102 ± 5 vs 99 ± 8 [SD] mm Hg, hypertensive vs control dogs) and intraocular pressure (18.1 ± 2.5 ys 17.7 ± 2.1 mm Hg, hypertensive vs control dogs) were similar in both groups. In normotensive control dogs, mean arterial pressure and intraocular pressure averaged over the postoperative period (4–8 weeks) did not differ significantly from preoperative values. In contrast, during the same period arterial pressure significantly increased and intraocular pressure significantly decreased in hypertensive dogs (arterial pressure, 163 ± 8 mm Hg; intraocular pressure, 11.9 ± 4.0 mm Hg;p< 0.001 for both values compared with corresponding values in control dogs). Intraocular pressure was inversely related to arterial pressure in hypertensive dogs (r = 0.56,p< 0.01). These observations indicate that intraocular pressure decreases with the development of canine one-kidney, one wrapped hypertension. The mechanism of this decrease may be related to abnormalities in Na+, K+-adenosine triphosphatase activity found in this form of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Central dopaminergic mechanisms involved in the regulation of plasma aldosterone concentration were investigated in 16 conscious sheep following Na depletion with intramuscularly administered furosemide. Intracerebroventricular infusion of dopamine (20 μg/min) decreased plasma aldosterone significantly to 52 ± 8% of basal level and increased plasma renin activity (PRA) significantly to 172 ± 25% of basal level in this animal model. In addition, intracerebroventricular infusion of the dopamine antagonist metoclopramide (20 μg/min) in artificial cerebrospinal fluid vehicle significantly increased aldosterone levels to 144 ± 14% of basal level and decreased PRA to 62 ± 5% of basal value. Neither intracerebroventricular infusion of the vehicle nor intravenous infusions of metoclopramide or dopamine at the same doses changed aldosterone or PRA levels. Intracerebroventricular bolus injections of metoclopramide (20 μg/kg in 0.4 ml of vehicle) were also effective, increasing aldosterone levels to 266 ± 22% of basal level and decreasing PRA to 70 ± 12% of basal level. Intravenous bolus injections of the same dose of metoclopramide were ineffective. Dopamine was infused intracerebroventricularly into two uniadrenalectomized sheep with the remaining adrenal transplanted to the neck. Aldosterone levels were decreased to 49 ± 10% of basal level, and PRA was increased to 157 ± 10% of basal value. None of the infusions or injections changed arterial or intracranial pressure, or plasma K, Na, and cortisol levels. These data indicate that endogenous or exogenous dopamine may act on central dopamine receptors to decrease plasma aldosterone concentration by an unknown humoral mechanism. The known aldosterone regulators, plasma Na, K, angiotensin II, and adrenocorticotropic hormone, are not involved in the regulation.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Rabbits were rendered hypertensive by suprarenal coarctation of the abdominal aorta. Seven days later, endothelium-dependent and endothelium-independent vascular relaxations were examined in vascular rings taken from hypertensive (thoracic aorta, carotid artery) and normotensive (abdominal aorta) regions. Relaxation of phenylephrine-contracted rings in response to endotheliumdependent agonists (acetylcholine, A23187) was impaired, compared with that in sham-operated and intact controls, in regions exposed to the elevated blood pressure (i.e., above the coarctation). Responses to acetylcholine and A23187 in the abdominal aorta, below the coarctation, were not altered. The diminished endothelium-dependent responses in the thoracic aorta were not affected by pretreatment with the cyclooxygenase inhibitor indomethacin. In contrast to acetylcholine and A23187, responses to the endothelium-independent agonist nitroprusside were not attenuated in vessels from hypertensive regions, indicating that the defect occurred in the endothelium. The EC50for acetylcholine-induced relaxations of thoracic aorta correlated significantly with mean arterial pressure above the coarctation, indicating that the extent to which endothelium-dependent relaxation is impaired is in proportion to the degree of blood pressure elevation. This study suggests that the diminished relaxations by endothelium-dependent agonists is a local response to the elevation of blood pressure and is not due to a circulating factor.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The mammalian atrial hormone atrial natriuretic factor (ANF) has been shown to have potent natriuretic and diuretic actions as well as vasodilator effects when released into the circulation. To investigate how the levels of the circulating form of this peptide c$ cular fluid volume, we measured immunoreactive ANF in the plasm$ load, acute furosemide treatment, and chronic water restriction. Cii$ ANF increased significantly (p< 0.001) 1 minute after acute saline 1$ within 5 minutes. Volume contraction induced by furosemide treat$ significantly reduced the circulating immunoreactive ANF. These$ expansion causes an immediate release of immunoreactive ANF intt$ volume contraction results in a decline of circulating levels of imm$ tained during chronic volume contraction. These results suggest t$ intravascular fluid volume and respond by changing the levels of A$ and thereby participate in the regulation of body fluids and, perl$.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To support our contention that the Wistar-Furth rat is resistant to mineralocorticoid hypertension, we assessed the effects of deoxycorticosterone (DOC) administration or renal artery stenosis on the development of hypertension in the Sprague-Dawley and Wistar-Furth rat strains. Weekly administration of mineralocorticoid in the form of DOC pivalate resulted in rapid, severe hypertensive cardiovascular disease in Sprague-Dawley rats. Within 5 weeks the mean conscious systolic blood pressures in steroid-treated and control rats were 186 ± 4 and 118 ± 5 mm Hg, respectively. In contrast, blood pressures of Wistar-Furth rats were only moderately elevated, even after 10 weeks of DOC pivalate administration (136 ± 2 vs 116 ± 2 mm Hg for controls). Furthermore, none of the steroid-treated Wistar-Furth animals exhibited cardiovascular lesions. In parallel studies, littermates of these rat strains were subjected to renal artery stenosis and blood pressures were determined weekly in conscious rats. Silver clip constriction of the left renal artery, in the presence of the contralateral kidney, resulted in a rapid, sustained elevation of blood pressure in both Sprague-Dawley and Wistar-Furth rat strains (177 ± 4 and 176 ± 5 mm Hg, respectively). Corticosteroid levels were also determined in DOC-treated Sprague-Dawley and Wistar-Furth rats. The regimen employed resulted in a 10-fold increase in DOC levels as compared with controls, and the levels achieved were comparable in both strains. Thus, the Wistar-Furth rat appears to be selectively resistant to mineralocorticoid hypertensive vascular disease and thus affords a model for studying mechanisms of steroid hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Captopril facilitates detection of unilateral renovascular hypertension by selectively reducing glomerular filtration rate in affected kidneys. To determine if volume depletion augments this response, we compared the effects of captopril, furosemide, and combined furosemide plus captopril on individual kidney computer-derived clearances of99mTc-diethylenetriamine pentaacetic acid (DTPA) and [l31I] o-iodohippurate in two-kidney, one clip Goldblatt hypertensive rats and normal controls. In clipped kidneys, captopril reduced DTPA clearance significantly from baseline (from 0.31 ± 0.02 to 0.19 ± 0.04 ml/min/100 g;p< 0.02) whereas furosemide alone had no effect (0.28 ± 0.03 ml/min/100 g). Combined furosemide plus captopril further reduced clipped kidney DTPA clearance to a level significantly less than captopril alone (0.10 ± 0.02 ml/min/100 g;p< 0.02). Clipped kidney o-iodohippurate clearance was not changed from baseline by any treatment. In contralateral undipped and normal kidneys, DTPA clearance did not decline from baseline following either captopril or furosemide plus captopril treatment. Since the dose of captopril used (3 mg/kg by intraperitoneal injection) did not reduce systolic blood pressure of hypertensive rats significantly, these changes probably reflect intrarenal rather than systemic hemodynamic effects of converting enzyme inhibition and are consistent with the hypothesis that captopril interferes with glomerular nitration in stenotic kidneys by reducing efferent arteriolar vascular resistance. Prior volume depletion accentuates the effect of captopril on stenotic kidney glomerular filtration rate, providing improved functional discrimination of stenotic kidneys from contralateral undipped and normal kidneys. These results indicate that furosemide-induced volume depletion may increase the diagnostic sensitivity of captopril-enhanced WmTc-DTPA renography in the detection of unilateral renovascular hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Adenosine may be a physiological modulator of vascular smooth muscle tone, sympathetic neurotransmission, renin release, and renal and cardiac function. To facilitate the elucidation of the physiological role of adenosine, a microassay for adenosine was developed that allows accurate quantitation of adenosine in 75 μl of rat plasma, thus permitting multiple determinations of plasma adenosine levels in an individual rat without inducing hemodynamic perturbations due to blood loss. The technique employs a simple and rapid extraction of plasma with a reverse-phase Sep-Pak cartridge and exploits the increased mass sensitivity of microbore high performance liquid chromatography. The assay was verified by demonstrating 1) a linear relationship between the amount of adenosine added to plasma and the amount detected by the assay, 2) a linear relationship between the rate of adenosine infusion into rats and plasma adenosine levels, and 3) the absence of measurable adenosine levels in plasma incubated with adenosine deaminase. The mean arterial plasma level of adenosine in the anesthetized rat was determined to be 119 ± 28 (SD) ng/ml (n = 10). With the use of this assay, renal venous plasma levels of adenosine were found to be elevated sixfold in two-kidney, one clip Goldblatt hypertensive rats (1 week postclipping) compared with sham-operated controls. Given the known effects of adenosine on renin release, these data support a role for endogenous adenosine as a regulator of renin release in renovascular hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The link between dietary salt intake and the development of hypertension in the saltsensitive Dahl strain of rats remains elusive. There is evidence that Dahl salt-sensitive rats (DS) produce less vasodilator and natriuretic prostaglandins in response to salt loading than do control saltresistant rats (DR), although the reason for this blunted response is unknown. We examined the effects of chronic dietary salt loading on the plasma levels of nonesterified fatty acids in DS and DR. Animals were fed the same chow containing either 0.4% or 4% NaCl (wt/wt). At 12 weeks, 75 jul of tail capillary blood was obtained from restrained, conscious rats, and principal nonesterified fatty acids were measured by high performance liquid chromatography. Total nonesterified fatty acids rose in the 15 DR on high salt diets compared with values in 11 rats eating low salt (0.57 ± 0.05 vs 0.35 ± 0.01 mM;p< 0.001). The greatest changes occurred in levels of arachidonic acid (+ 287 %) and in the arachidonic precursors, linoleic (+ 89%) and linolenic (+107%) acids. In marked contrast, there was no change in levels of plasma nonesterified fatty acids in DS fed 4% NaCl compared with DS fed 0.4% NaCl. These observations suggest that defective production of natriuretic and vasodilator prostaglandins by DS may be due in part to an inability to produce or release eicosanoid precursors from phospholipid stores in response to dietary salt.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID