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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma parathyroid hormone (pPTH) levels have been assessed in three separate radioimmunoassay systems in samples from Wistar-Kyoto rats. The animals were subjected to one of three dietary regimens throughout the study period: Group 1 animals consumed normal rat chow and drank tap water; Group 2 animals consumed normal rat chow and tap water was replaced with 0.5% saline solution; Group 3 animals consumed normal rat chow to which 2.5% CaCO3 (by weight) had been added and also drank 0.5% saline solution. Animals had consumed these diets for approximately 7 months prior to sacrifice for blood collection. Blood pressure was measured by tail cuff plethysmography in these animals and, as previously reported, saline consuming animals showed a moderate hypertension (Gp 2) only when diets did not contain added calcium (Gp 3). In the week prior to sacrifice, mean blood pressures were: Gp 1: 128.0 +/- 3.46 mmHg; Gp 2: 140.2 +/- 3.15 mmHg; and Gp 3: 133.5 +/- 2.90 mmHg. Three assay systems were used to measure pPTH levels from trunk blood samples obtained by guillotine decapitation. One assay used an antiserum directed toward the vasoactive N terminal fragment 1-34 and produced pPTH measurements of 0.74 +/- 0.05 ng/ml in Gp 1 animals, 1.04 +/- 0.07 ng/ml in Gp 2 animals and 1.12 +/- 0.08 ng/ml in Gp 3 animals. This pattern was consistent with that obtained by another antiserum which had been raised against the intact 1-84 PTH molecule and produced values of 0.25 +/- 0.03 ng/ml in Gp 1 animals, 0.55 +/- 0.07 ng/ml in Gp 2 animals and 0.74 +/- 0.04 ng/ml in Gp 3 animals. Antiserum raised against the C-terminal did not show any difference in pPTH across groups. We conclude that saline consumption may increase some portions of circulating PTH. Such elevation of pPTH may not be a pathophysiological component in the sodium dependent elevation of blood pressure since animals concurrently consuming both saline and calcium supplemented diets retained elevated pPTH levels even though blood pressures did not differ from controls. Rather, elevation of circulating PTH levels may be a response to prolonged increases in sodium consumption.
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PMID:Parathyroid hormone in sodium-dependent hypertension. 362 62

Aortic potassium turnover was studied during the development of hypertension induced by salt load in male rats after 70-75% of total renal mass was removed. Systolic blood pressure in the saline-drinking experimental reduced renal mass (RRM) rats steadily increased until the fourth week after surgery and thereafter stayed at the same level. Control RRM rats given tap water for drinking, and unilaterally nephrectomized saline-drinking control rats maintained normal blood pressure. Compared to controls, experimental RRM rats exhibited increased plasma aldosterone concentration while plasma renin activity was low in all groups with no significant difference. Aortic hypertrophy, greater 42K turnover, and elevated 42K exchange were observed with experimental RRM hypertension. Sensitivity to the effect of norepinephrine (NE) on aortic 42K turnover was increased four- to ninefold in the experimental RRM group as compared to controls. These results indicate that reduced renal mass hypertension is associated with increased potassium permeability and NE supersensitivity in vascular smooth muscle.
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PMID:Increased arterial potassium transport in reduced renal mass hypertension of the rat. 370 75

The dynamics of hypothalamic arginine vasopressin (AVP) release was examined during the development of hypertension in rats with deoxycorticosterone (DOCA)-NaCL induced hypertension. Experiments were performed in four groups of uninephrectomized Sprague-Dawley rats 3, 7, 14 and 21 days after treatment with: (I) DOCA and 1% saline (DOCA-NaCl); (II) DOCA, regular chow, and tap water (DOCA-R-H2O); (III) regular chow and 1% saline (NaCl); and (IV) regular chow and tap water (H2O). Systolic blood pressure (BP) was significantly elevated in DOCA-NaCl and DOCA-R-H2O (183 +/- 5 and 155 +/- 4 mm Hg, respectively) but not in an additional control group which received DOCA and a low NaCl diet (119 +/- 2 mm Hg). Plasma AVP and hypothalamic AVP release were increased in all DOCA treated groups at each time point studied, while plasma osmolality was similar in each group. These studies demonstrate increases in the hypothalamic release of AVP in DOCA-NaCl hypertensive animals, but suggest that they are due to the mineralocorticoid and are independent of blood pressure and NaCl intake.
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PMID:Increased vasopressinergic activity following DOCA administration in the rat. 395 90

Normotensive female Wistar Kyoto rats were studied to examine the effects of replacing drinking water with highly palatable saline solution at a concentration (0.5%) close to the maximum preferred concentration in these animals. A further group of animals was offered a calcium-supplemented diet in addition to substitution of drinking water with saline. Fluid consumption in animals drinking tap water was constant at between 35-40 ml/day throughout the six-month study period. In contrast, animals drinking 0.5% saline consumed 75-85 ml/day throughout the study period, irrespective of the calcium content of the diet. Voluntary consumption of these quantities of saline was associated with the development of a moderate hypertension, measured by tail cuff plethysmography, after two months of study. However, in animals consuming calcium-supplemented diets the hypertensive response disappeared after 3 months of study. Blood pressures were validated at the conclusion of the study by direct arterial cannulation and confirmed the presence of hypertension in saline drinking animals only when diets lacked calcium supplementation. No changes in blood ionized sodium concentration were associated with saline consumption; however, blood ionized calcium was significantly reduced in animals drinking saline, but not when calcium-supplemented diet was available. These studies suggest an interaction between sodium and calcium in the genesis of sodium-dependent hypertension.
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PMID:Sodium and hypertension: effect of dietary calcium supplementation on blood pressure. 407 43

In 14 patients with supratentorial tumours and symptoms of intracranial hypertension the concentrations of HVA and 5-HIAA were determined in cerebrospinal fluid obtained by lumbar tap. Significantly raised levels of both these metabolites were demonstrated in the cerebrospinal fluid in these patients in relation to controls. The cause of this rise could be excessive production of serotonin or dopamine, increased turnover of these amines or impaired absorption of 5-HIAA and HVA by the choroid plexus of the fourth ventricle.
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PMID:[Homovanillic (HVA) and 5-hydroxyindoleacetic (5-HIAA) acid concentration in the cerebrospinal fluid of patients with supratentorial tumors and symptoms of intracranial hypertension (preliminary report)]. 615 3

In rats with deoxycorticosterone acetate (DOCA) salt hypertension, induction of diabetes with streptozotocin did not aggravate the elevation in blood pressure, but pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were enhanced. Along with glycosuria and hyperglycemia, the other effects of streptozotocin-induced diabetes were: reduced body weight, increased fluid intake, and bradycardia. Despite enhanced responsiveness to hypothalamic stimulation, blood pressure increases produced by intravenous injections of norepinephrine, tyramine, or vasopressin were unaltered. When pressor responses were compared in diabetic rats drinking either tap water or isotonic saline solution, no appreciable differences occurred. It was considered possible that hypothalamic responsiveness was enhanced in diabetic-DOCA hypertensive rats by increases not only in sympathetic nerve firing but also in release of endogenous norepinephrine.
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PMID:Hypothalamic responsiveness in DOCA hypertensive rats augmented by streptozotocin-induced diabetes. 618 70

The control of hypertension with antihypertensive agents, in the spontaneously hypertensive rats (SHR) can result in regression of established cardiac hypertrophy. This study compared the effects of therapy with oxprenolol (Ox) and with hydrochlorothiazide (Htz) for (1) regression of established left ventricular hypertrophy (LVH) and (2) blood pressure control. Three groups of SHR and 3 comparable groups of Wistar-Kyoto (WKY) rats, matched for age, sex and body wt, were treated with tap water (Gp I), 60-200 mg hydrochlorothiazide kg-1 day-1 (Gp II) and 15-500 mg oxprenolol kg-1 day-1 (Gp III) for 13 weeks. Systolic and diastolic blood pressures (SBP, DBP mmHg), left ventricular wt/body wt ratio (LVwt/Bwt mg g-1) and left ventricular wall thickness (LVWT mm) were recorded. Oxprenolol lowered both systolic (mean +/- S.E. mmHg, 130 +/- 7 vs 189 +/- 8; P less than 0.01) and diastolic blood pressures (mean +/- S.E. mmHg, 104 +/- 6 vs 159 +/- 6; P less than 0.001) and caused regression of left ventricular hypertrophy (mean +/- S.E. mg g-1, 2.91 +/- 0.06 vs 3.10 +/- 0.09; P less than 0.05). In contrast, hydrochlorothiazide did not control blood pressure (mean +/- S.E. mmHg, 183 +/- 5 vs 189 +/- 6 and 152 +/- 5 vs 156 +/- 6), but it did cause regression of left ventricular hypertrophy (mean +/- S.E. mg g-1, 2.67 +/- 0.03 vs 3.10 +/- 0.09; P less than 0.01). Left ventricular wall thickness, measured in the mid-ventricular region, was significantly reduced only by hydrochlorothiazide (mean +/- S.E. mm, 2.76 +/- 0.06 vs 3.21 +/- 0.01; P less than 0.05). These results suggest that regression of left ventricular hypertrophy can occur with or without control of hypertension in the SHR.
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PMID:Regression of left ventricular hypertrophy and control of hypertension in the spontaneously hypertensive rat (SHR): oxprenolol versus hydrochlorothiazide. 621 50

1. Altered adrenergic responsiveness of hearts and blood vessels occurs in both experimental and clinical hypertension. 2. Since salt excess aggravates both types of hypertension, we investigated beta-adrenoreceptor properties in the hearts of spontaneously hypertensive and normotensive rats drinking 1% NaCl or tap water for 3 weeks. 3. Sodium loading increased heart weight in both spontaneously hypertensive and normotensive rats. 4. In spontaneously hypertensive rats excess salt attenuated the age-related decrease in beta-adrenoreceptor number observed in spontaneously hypertensive and normotensive rats drinking tap water and in normotensive rats drinking 1% NaCl. 5. Unlike the normotensive rats, which did not show a relationship between beta-adrenoreceptor number and blood pressure, spontaneously hypertensive rats on tap water and 1% NaCl showed a significant negative logarithmic relationship between these two variables. These data provide further evidence implicating sodium excess as an aggravating factor in this model of experimental hypertension.
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PMID:Altered cardiac beta-adrenoreceptors in spontaneously hypertensive rats receiving salt excess. 625 10

Vanadate, a potent naturally occurring Na+,K+-ATPase inhibitor thought to have a role in regulating Na+-K+ pump activity, was fed to uninephrectomized rats drinking tap water or a 1% solution of sodium chloride for as long as 56 weeks. Feeding was achieved by adding sodium orthovanadate to normal rat chow equivalent to 100 or 200 ppm vanadium by weight. In the rats drinking tap water, systolic pressure gradually increased over a period of several weeks and then was sustained in a dose-related manner for the duration of the treatment. The increased pressure was not associated with changes in water intake, urine output, or urinary sodium excretion but correlated positively with plasma vanadium levels ranging from 0.04 to 0.27 microgram/ml. Increased pressure was associated with increased heart-to-body-weight ratio but did not appear to occur in a small group of animals drinking the 1% solution of sodium chloride. These findings, considered in the light of others, indicate that vanadate deserves continued study in relation to hypertension.
Hypertension
PMID:Effect of prolonged dietary administration of vanadate on blood pressure in the rat. 626 56

Central catecholamine (CA) neurons in the nucleus tractus solitarius (NTS) and paraventricular hypothalamic nucleus (PVN) were studied in Wistar rats that had been unilaterally nephrectomized. The experimental animals were then treated with deoxycorticosterone acetate (DOCA) and salt water. The control animals were treated with the vehicle and tap water. Blood pressure of animals 4 weeks after DOCA/salt treatment was significantly elevated when compared to control rats. Morphologically, CA terminals showed no noticeable changes in the DOCA/salt hypertensive rats. Furthermore, the density of CA terminals either in the NTS or in the PVN of the DOCA/salt hypertensive rats was not statistically different from that of normotensive controls, suggesting that salt does not cause lesions or destruction of CA terminals. However, an extensive electron-microscopic morphometric analysis indicated that there was an enhancement of CA synaptogenesis (expressed by increased synaptic frequency among all CA boutons labeled with 5-hydroxydopamine) in the PVN, but not in the NTS of DOCA/salt hypertensive rats. In addition, the high-performance liquid chromatography revealed decreased CA contents in the PVN, but not in the NTS, of DOCA/salt hypertensive animals. Since synapses are primary sites for neurotransmitter release, the above results collectively suggest that more CA synapses formed in the PVN may reflect a net CA release from CA terminals resulting in the decreased CA content in the axonal terminals. Such an increased CA release and enhanced CA synaptogenesis may consequently enhance CA function in the PVN of hypertensive rats 4 weeks after DOCA/salt treatment, and relate to the development and/or maintenance of hypertension in the DOCA/salt rats.
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PMID:Catecholamine synapses and contents in the paraventricular hypothalamic nucleus and nucleus tractus solitarius of DOCA-salt hypertensive rats. 647 21


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