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PubMed1986

Effects of hydralazine on blood pressure, pressor mechanisms, and cardiac hypertrophy in two-kidney, one-clip hypertensive rats.

In 2-kidney, 1-clip hypertensive rats, the time course of changes in blood pressure (BP), heart rate, activity of the sympathetic nervous system and the renin-angiotensin system, plasma and blood volumes, left ventricular (LV) and right ventricular (RV) weight, and LV dimensions were evaluated during treatment with hydralazine 80 and 120 mg/L drinking water for 2 days or 1, 2, 3, 5, and 8 weeks. Hydralazine induced initially a clear antihypertensive effect (mean BP from 170-180 down to 135-145 mmHg (1 mmHg = 133.32 Pa], subsequently tolerance developed. Heart rate, plasma catecholamines, and the blood pressure response to hexamethonium were not affected by treatment. Significant increases in plasma renin activity occurred during the initial 1-3 weeks of treatment. Plasma and blood volumes showed only small increases with prolonged treatment. RV weight and LV internal diameter showed significant increases at 3, 5, and 8 weeks of treatment, LV weight at 5 and 8 weeks. LV wall thickness did not change significantly. Thus, treatment with the arterial vasodilator hydralazine causes both RV hypertrophy and eccentric LV hypertrophy. Intravascular volume expansion, associated possibly with redistribution of blood volume to the central compartment, may play a major role in these cardiac effects. Increased renin release but not a generalized increase in sympathetic tone may play a role in the development of tolerance to the antihypertensive effect.

Animals↗
PubMed1994

Effects of acupuncture on blood pressure and plasma renin activity in two-kidney one clip Goldblatt hypertensive rats.

Shih-Hsüan [Sipseon (EX-UE-11)] are Curious loci lying outside of the meridians on the tips of each finger. These loci have long been the acupuncture sites for the treatment of cardiovascular disease in oriental medicine. Alterations in the renin-angiotensin system have been considered as the pathophysiological basis of the origin and/or maintenance of hypertension. Activation of the plasma or tissue renin-angiotensin system may be one of the cause of hypertension. The aim of the present study was to elucidate the effects of acupuncture on blood pressure and plasma renin activity. Acupuncture was applied on the EX-UE-11 of two-kidney one clip Goldblatt hypertensive rats. Both the systolic blood pressure and the plasma renin activity decreased significantly after treatment with acupuncture on the EX-UE-11. In the sham-operated and control rats, the procedure influenced the parameters without significant changes. The results suggest that the suppressive hemodynamic effect of acupuncture on the EX-UE-11 may be related to changes in plasma renin activity.

Acupuncture Therapy↗
PubMed1979

Advances in radiologic reporting with Computerized Language Information Processing (CLIP).

Computerized Language Information Processing (CLIP) is a system of radiologic reporting in which the user interacts with a computer keyboard and cathode-ray tube terminal to generate coded reports. The hierarchical medical classification on which the code is based permits rapid on-line compilation of reports of any degree of complexity. The system provides organized sets of pre-assembled statements that are rapidly accessed and modified for each examination. Although the reports are printed in English, they are held in the computer as a succinct code that is eminently suited for permanent storage and rapid retrieval.

Classification↗
PubMed1991

Insulin resistance and blood pressure in Dahl rats and in one-kidney, one-clip hypertensive rats.

In normal rats, sucrose feeding results in insulin resistance and an elevation of arterial pressure. The purpose of this study was twofold: 1) to evaluate the effect of sucrose feeding on blood pressure in a genetic model and in an acquired model of hypertension and 2) to determine whether these models of hypertension are associated with insulin resistance. In Dahl salt-resistant (Dahl-R) rats on both a 0.45 and a 3% NaCl intake, systolic blood pressures were higher (P less than 0.01) in sucrose-drinking than in water-drinking animals. In contrast, blood pressure was not affected by dietary sucrose in Dahl salt-sensitive (Dahl-S) rats. Blood pressure was also not affected by sucrose in the one-kidney, one-clip (1K,1C) hypertensive rat. In response to an oral glucose load, serum glucose was similar in Dahl-R and Dahl-S rats, although serum insulin was higher (P less than 0.05) in Dahl-S rats, suggesting that Dahl-S rats are insulin resistant. In contrast, glucose and insulin responses were similar in hypertensive 1K,1C animals and normotensive controls. In conclusion, sucrose feeding increased blood pressure in Dahl-R but not in Dahl-S or 1K,1C hypertensive rats. Additionally, Dahl-S rats, but not hypertensive 1K,1C rats, are insulin resistant.

Animals↗
PubMed1983

Decreased myocardial Na+-K+-ATPase activity in one-kidney, one-clip hypertensive rats.

We have previously shown that Na+-K+ pump activity (ouabain-sensitive 86Rb uptake) is decreased in vascular tissue of animals with various forms of low renin hypertension. In the present study we measured Na+-K+-ATPase activity, the energy source for Na+-K+ pumping, in membrane fractions prepared from myocardial tissue of rats with chronic one-kidney, one-clip hypertension and their one-kidney normotensive controls. Membranes were prepared by two independent methods: microsomal fractions (method 1) and fractions prepared by the hypotonic LiBr method of Dhalla et al. (method 2). In membranes prepared from left ventricles of the hypertensive rats (by method 1) Na+-K+-ATPase activity was decreased, Mg2+-ATPase activity was increased, and the sialic acid content and 5'-nucleotidase activity (two putative membrane markers) were unchanged relative to the control rats. The sensitivity of cardiac Na+-K+-ATPase to inhibition by ouabain was also unchanged. Na+-K+-ATPase activity was also decreased in the right ventricles (method 1) of these hypertensive rats, suggesting that this defect is probably not pressure related. In membranes prepared from the left ventricles of the hypertensive rats by method 2, Na+-K+-ATPase activity was again reduced, whereas the Mg2+-ATPase and 5'-nucleotidase activities were unchanged relative to the controls. These studies suggest that myocardial Na+-K+-ATPase activity is suppressed in rats with this low renin form of hypertension and the possible effect of this suppression on myocardial contractile activity is discussed.

5'-Nucleotidase↗
PubMed1984

Microvascular alterations in the one-kidney, one-clip renal hypertensive rat.

The microcirculation was studied in one-kidney, one-clip renal hypertensive rats ( 1KG ) and uninephrectomized controls at 4-6 and 8-10 wk postoperation. Under chloralose-urethan anesthesia the gracilis muscle was transilluminated in situ with a light pipe. Measurements of arteriolar and capillary density and arteriolar diameter were made in three consecutive states: innervated, denervated, and vasodilated with nitroprusside. Arteriolar wall-to-lumen ratio was measured after vasodilation. At 4-6 wk vasoconstriction was significantly greater in 1KG and vasodilated arteriolar diameter was significantly smaller, partially because of an elevated wall-to-lumen ratio. Capillary density in 1KG was reduced in the innervated and denervated states compared with controls. At 8-10 wk in the 1KG , arteriolar vasoconstriction was no longer significantly elevated. However, the vasodilated arteriolar diameter was smaller, wall-to-lumen ratio had increased further, and rarefaction of arterioles and capillaries was present. Thus, with time, structural mechanisms for increasing vascular resistance were seen to displace the active mechanism of vasoconstriction.

Animals↗
PubMed1984

Hypertension after ending captopril administration: pathogenesis in 2-kidney, 1-clip rat.

We have previously shown that continuous captopril administration prevents hypertension from developing in the two-kidney, one-clip (2K, 1C) rat. The present investigation was designed to determine the mechanism(s) producing the hypertension. In one series of experiments captopril prevented pressure from increasing during an 8-wk treatment period. Relative to the last day of treatment, mean arterial pressure and total peripheral resistance (TPR) were increased and cardiac output was unchanged at 3, 7, and 28 days after captopril cessation. Plasma renin activity (PRA) was unchanged 3, 7, and 14 days after captopril cessation but was elevated at 28, 49, and 56 days after captopril cessation only in 2K, 1C rats with severe hypertension (systolic blood pressure greater than 180 mmHg). Guanethidine (45 mg/kg po, bid) did not prevent the development of 2K, 1C hypertension but did prevent the hypertension from developing after cessation of captopril. Blockade of the prostaglandin system with indomethacin (5 mg/kg + 50 micrograms X kg-1 X min-1) and of the kallikrein-kinin system with aprotinin (25,000 KIU + 150 KIU X kg-1 X min-1) for 2 h had no effect on captopril's antihypertensive effect. Additionally, no change in sodium or water balance was observed after captopril cessation. Taken together these data demonstrate that hypertension after captopril cessation is due to an increase in TPR. Additionally, the rise in TPR is due to both the sympathetic nervous and the renin-angiotensin systems since both systems must be functional before pressure rises.

Animals↗
PubMed1985

Arteriolar responses to norepinephrine and ouabain in early 1-kidney, 1-clip hypertension in rats.

We assessed the role of putative circulating ouabainlike factors on in vivo arteriolar function in rats with very early (less than or equal to 7 days, mean 3 days), benign, one-kidney, one-clip (1K1C) hypertension. Thus we measured vascular responses in vasodilated (nitroprusside or adenosine), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized 1K1C rats perfused with their own blood at 1 ml/min. Complete dose-response curves to norepinephrine in 19 1K1C compared with 25 uninephrectomized (1K) normotensive control rats showed unchanged thresholds and 50% effective dosages. Magnitude of ouabain-induced leftward shifts of the dose-response curve in 29 1K1C and 30 1K rats were similar. In 1K1C, compared with 1K, limb resting resistance was elevated by 45% (P less than 0.001), and limb resistance at maximal vasodilation was elevated by 15% (P less than 0.02). These results provide no evidence in this form and stage of hypertension that humoral ouabainlike inhibitors of the sodium-potassium pump evoke physiologically significant inotropic effects in arterioles in vivo. However, the results suggest that significant increases in arteriolar wall-to-lumen ratio occur in the earliest stages (3 days) of hypertension and probably contribute to the elevated resistance.

Animals↗
PubMed1987

Alterations in the microvasculature of one-kidney, one-clip hypertensive rats.

The microcirculation was studied in the cremaster muscle of one-kidney, one-clip (1K-1C) hypertensive rats and uninephrectomized controls under chloralose-urethan anesthesia 1-2, 4-5, or 8-9 wk following renal artery stenosis. With the use of television microscopy, inside and outside diameters of first (1A) through fourth-order (4A) arterioles were measured before and after vasodilation with 10(-4) M adenosine. Mean arterial blood pressure was significantly elevated in the 1K-1C rats, rising to 170 +/- 6 mmHg by 8-9 wks vs. 93 +/- 2 mmHg in controls. Enhanced vasoconstriction, resulting in closure of arterioles, appeared only in the smaller arterioles of 1K-1C and diminished throughout the development of hypertension. Structural rarefaction appeared later and increased with the development of hypertension. Vasodilated inside diameters of control, but not 1K-1C, 1A, 2A, and 3As, increased with increasing age, leaving the hypertensive arterioles with structurally reduced lumens and increased wall-to-lumen ratios, but without increases in wall cross-sectional areas. Structural lumen reduction appeared first in the 1A and advanced downstream as hypertension developed. Thus vasoconstriction of the smallest arterioles is important initially in renal hypertension, but structural alterations become more important later.

Adenosine↗
PubMed1987

Atrial natriuretic factor in dogs with one-kidney, one-clip Goldblatt hypertension.

The temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (ANF) were studied in dogs (n = 5) before and after renal artery constriction to produce one-kidney, one-clip renovascular hypertension. Three days after renal artery constriction, circulating ANF increased from 34 +/- 7 to 344 +/- 129 pg/ml (P less than 0.05) in association with a 38-mmHg elevation of mean arterial pressure and increases in plasma renin and aldosterone levels. Plasma renin and aldosterone remained elevated for 9 days after renal artery constriction. Arterial pressure stabilized at this elevated level of 35-40 mmHg above base line for the duration of the 4 wk after renal artery constriction. Right atrial filling pressure did not change significantly (P greater than 0.05) after constriction of the renal artery. This observation suggests that volume expansion with right atrial distention is not the only stimulus for release of ANF in these hypertensive dogs. Plasma ANF remained significantly elevated above base-line levels for 7 days postconstriction even though a twofold decrease from the maximal response of 344 +/- 129 pg/ml on day 3 to 168 +/- 48 pg/ml on day 7 was observed during this same time interval. Plasma ANF continued to decrease toward prehypertensive levels throughout the remainder of the established phase of the hypertension lasting an additional 21 days of observation. The mechanisms for this observed pattern of plasma ANF are unclear but may involve changes in left atrial distention and stretch as a stimulus for hormone secretion with progression of the hypertension.

Aldosterone↗
PubMed1988

Dexamethasone attenuates reversal of hypertension in one-kidney, one-clip rats.

This study examines the effect of dexamethasone (Dex), a phospholipase A2 inhibitor, on the reversal of 1-kidney, 1-clip (1K,1C) hypertension and the synthesis of phospholipase A2-dependent products. Male Sprague-Dawley 1K,1C hypertensive rats [blood pressure (BP) greater than 190 mmHg] were allocated to three groups: two groups were given daily oral doses of Dex (0.142 mg/kg in water) for 72 h, whereas the third group was given water only (controls). One of the Dex-treated groups was then sham unclipped (n = 9), while the other Dex-treated group (n = 8) and the control group (n = 8) were unclipped. Dex attenuated the BP fall in the unclipped (223 +/- 8-148 +/- 9 mmHg) compared with the control unclipped (226 +/- 9-114 +/- 5 mmHg) animals (P less than 0.005). Aortic 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) was reduced in unclipped Dex-treated rats (13.4 +/- 1.2 ng/mg) compared with unclipped control rats (16.3 +/- 1.4 ng/mg; P less than 0.05) but was higher than in the sham-unclipped Dex group (11.5 +/- 1.2 ng/mg; P less than 0.05). Serum thromboxane B2 (TxB2) in the unclipped Dex-treated group was lower than in the unclipped control rats (P less than 0.05) but higher than in sham-unclipped rats (P less than 0.05). Dex significantly increased urinary prostaglandin E2 (PGE2) excretion, whereas urinary 6-keto-PGF1 alpha was unaltered. After unclipping, both urinary PGE2 and 6-keto-PGF1 alpha increased significantly, although there was no obvious difference between Dex-treated and control animals. These findings demonstrate opposite effects of Dex on renal compared with extrarenal prostanoid synthesis and support the hypothesis that attenuation of aortic 6-keto-PGF1 alpha synthesis may be responsible for the smaller fall in BP after unclipping in Dex-treated rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Angiotensin-dependent renal mechanisms in two-kidney, one-clip renal vascular hypertension.

Our understanding of the physiology of the renin-angiotensin system has advanced remarkably in the last decade as a result of the development of several pharmacologic agents that effectively block components of this humoral cascade. The use of these antagonists has also advanced our understanding of the contribution of the renin-angiotensin system to the development and maintenance of two-kidney, one-clip renal vascular hypertension. These antagonists have contributed greatly to the characterization of the systemic hemodynamic changes that occur in this model and, particularly, to the delineation of the behavior of the nonclipped kidney, a previously normal kidney that is subjected acutely to an environment of elevated systemic blood pressure and the input of a variety of other extrinsic influences. This kidney not only allows the blood pressure to increase and persist at elevated levels but appears to actively participate in the development and propagation of the hypertension. Although a variety of mechanisms impinge on the function of the nonclipped kidney in this model, the goal of this review is to analyze the behavior of this kidney and how its functional state is perturbed, primarily by the influence of angiotensin, which is believed to be delivered to it by the systemic circulation.

Animals↗
PubMed2001

Infectious aneurysm clipping by an MRI/MRA wand-guided protocol. A case report and technical note.

Infectious aneurysms are potentially deadly sequelae of multiple etiologies, typically associated with subacute bacterial endocarditis (SBE). Since these aneurysms tend to be distal, there are no consistent landmarks by which to localize them, in contrast to more typical aneurysms that occur on the circle of Willis or proximal, large cerebral vessel bifurcations. In addition, they tend to be extremely friable and may be obscured by blood if intracranial hemorrhage (ICH) has already occurred. These factors make clipping these aneurysms technically difficult, and searching for easily ruptured aneurysms without standard landmarks adds risk to the procedure. In this report, we describe the case of a 9-year-old boy with SBE and subsequent ICH secondary to a mycotic aneurysm. This aneurysm was localized to within millimeters by the MRI protocol described herein. The aneurysm was excised and the patient recovered without incident. Thus, MRI/MRA-guided frameless stereotaxy may be useful for localizing distal mycotic aneurysms, improving patient outcome by decreasing morbidity and mortality.

Aneurysm, Infected↗
PubMed2003

Effect of endothelin blockade on early cardiovascular remodeling in the one-clip-two-kidney hypertension of the rat.

BACKGROUND: In models of hypertension and of renal failure, pharmacological blockade of the ET(A) receptor has been shown to cause some inconsistent lowering of blood pressure (BP) and lesser left ventricular hypertrophy (LVH). The effects of ET(A) receptor blockade (ET(A)-RB) on vascular remodeling and their potential relation to BP lowering, have not been clarified. DESIGN: The experimental study in male Sprague-Dawley rats was designed to compare four experimental groups: (1) sham-operated controls (sham); (2) untreated rats with one-clip-two-kidney (1C-2K) renovascular hypertension; (3) 1C-2K rats treated with the ACE inhibitor (ACE-i) trandolapril (0.3 mg/kg b.w./day), and (4) 1C-2K rats treated with the ET(A)-RB LU-135252 (50 mg/kg b.w./day). BP was measured weekly by tail plethysmography. After 3 weeks, animals were sacrificed and cardiac, aortic and mesenteric artery morphology was evaluated using morphometric and stereological techniques. RESULTS: Systolic BP was significantly higher in 1C-2K rats compared to sham. BP was not significantly affected by ET(A)-RB, but was significantly lowered by the ACE-i. Despite no significant change in BP, ET(A)-RB treatment led to a significantly less volume density of the cardiac interstitium (sham 1.40 +/- 0.18, 1C-2K 2.66 +/- 0.56, 1C-2K + ACE-i 1.88 +/- 0.38, 1C-2K + ET(A)-RB 2.15 +/- 0.37%). In contrast, ET(A)-RB had no significant effect on left ventricular/body weight ratio (sham 2.85 +/- 0.26, 1C-2K 2.96 +/- 0.33, 1C-2K + ACE-i 2.54 +/- 0.22 and 1C-2K + ET(A)-RB 3.15 +/- 0.44 mg/g) or on wall thickness of intramyocardial arteries. CONCLUSIONS: The ET(A)-RB LU-135252 ameliorated the development of myocardial fibrosis in a short-term hyperreninemic normal salt model of experimental hypertension nearly as effectively as an ACE-i. This effect of LU-135252 is independent of systemic BP. In contrast to findings in other models, ET(A) receptor blockade had no significant effect on LVH or vascular remodeling. Only the ACE-i but not the ET(A)-RB prevented structural changes of small intramyocardial arteries and of the aorta.

Animals↗
PubMed2004

Relaxation induced by acetylcholine involves endothelium-derived hyperpolarizing factor in 2-kidney 1-clip hypertensive rat carotid arteries.

Acetylcholine induced relaxation in a concentration-dependent way in isolated phenylephrine-contracted carotid artery rings from normotensive two-kidney (2K) and hypertensive two-kidney one-clip (2K-1C) rats. In the presence of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NOARG, 100 micromol/l), the relaxation stimulated with acetylcholine was blocked in 2K arteries. However, in 2K-1C arteries, the relaxation was only partially inhibited. Indomethacin (3 micromol/l) had no effect in both groups. In 2K arteries, the combination of L-NOARG and indomethacin had similar effects to L-NOARG alone. On the other hand, in 2K-1C arteries, indomethacin further inhibited the maximum effect induced by acetylcholine. Endothelium-dependent relaxation induced by acetylcholine was markedly reduced in 2K arteries contracted with 90 mmol/l KCl, and it was abolished in 2K-1C arteries. The remaining response to acetylcholine in 2K arteries was blocked by L-NOARG. Thus, in addition to NO, a relaxing factor sensitive to extracellular K+ changes in the membrane potential contributes to endothelium-dependent relaxation in 2K-1C rat carotid artery. On the other hand, in arteries from 2K rats, only NO is involved in the relaxation induced by acetylcholine. The combination of 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, 3 micromol/l), indomethacin (3 micromol/l) and L-NOARG (100 micromol/l) reduced the relaxation induced by acetylcholine in arteries from 2K-1C rats contracted with phenylephrine. On the other hand, in 2K arteries, the relaxation induced by acetylcholine was abolished. The combination of ODQ and K+ channel blockers charybdotoxin (100 nmol/l), apamin (500 nmol/l) and 4-aminopyridine (1 micromol/l) abolished the relaxation induced by acetylcholine in 2K and 2K-1C carotid arteries. These data indicate that the endothelium-derived relaxing factors that contribute to relaxation induced by acetylcholine are different in 2K and 2K-1C arteries. In 2K arteries, the only factor is NO, which involves the activation of K+ channels and the cGMP pathway. However, in 2K-1C arteries, the relaxation induced by acetylcholine is dependent on NO in addition to another factor, which is insensitive to indomethacin, but also activates the K+ channels and the cGMP pathway, presumably by membrane hyperpolarization through endothelium-derived hyperpolarizing factor.

Acetylcholine↗
PubMed1982

Depressed adrenergic nerve function in tibial arteries of two-kidney one clip Goldblatt hypertensive dogs.

Tibial arteries removed from normotensive dogs and from two-kidney one clip Goldblatt hypertensive dogs, 6-34 days after renal artery constriction, were studied in vitro. Contractions were elicited by transmural stimulation and norepinephrine added to the organ bath. Arteries from the hypertensive dogs exhibited depressed responsiveness to adrenergic nerve stimulation, but not to the lower concentrations of norepinephrine. However, the maximal response to norepinephrine was decreased as has been previously observed in hypertensives' arteries. The results indicate that pre- and postsynaptic factors are involved in the depressed adrenergic responses in the hypertensives' tibial arteries.

Animals↗
PubMedDate not supplied

Mechanical properties of porcine small coronary arteries in one-kidney, one-clip hypertension.

The purpose of this study was to analyse the mechanical properties of small coronary arteries from pigs with one-kidney, one-clip hypertension and normotensive control animals and to determine whether these could contribute to vascular structural changes observed in hypertension. Small coronary artery wall tension-internal circumference relationships were determined for coronary arteries mounted in a myograph and used to calculate incremental elastic modulus-stress relationships for arteries from normotensive and hypertensive pigs. Wall tension-internal circumference relationships were shifted to the left in arteries from hypertensive pigs, but the stress-strain and incremental elastic modulus-stress relationships were not influenced by the increased blood pressure load. These data indicate that small coronary arteries from hypertensive pigs are not less distensible than those from normotensive controls. Therefore the previously reported increased media thickness:lumen diameter ratios in coronary arteries in this model of hypertension are not a consequence of abnormal elastic properties and can be ascribed to a remodelling process.

Animals↗