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1. |
Frottt the American Heart Association |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 8-27
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ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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2. |
Biotechnology and the Pharmaceutical Industry New Cardiovascular Drugs |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 965-970
MARK DIBNER,
PIETER TIMMERMANS,
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ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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3. |
Vasodepressor Role of Endogenous Bradykinin Assessed by a Bradykinin Antagonist |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 971-974
ATHANASSIOS BENETOS,
HARALAMBOS GAVRAS,
JOHN STEWART,
RAYMOND VAVREK,
SIMON HATINOGLOU,
IRENE GAVRAS,
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摘要:
This study was designed to examine the contribution of bradykinin to the depressor effect of different antihypertensive drugs in two-kidney renovascular hypertensive rats, using a new specific antagonist of bradykinin. First, the inhibitory capacity of this peptide for exogenously injected bradykinin (75–200 ng) was tested. An inhibition of the vasodepressor action of bradykinin by over 50% was found when the bradykinin inhibitor was infused at a rate of 40 μg/min, with little difference at higher rates of infusion. This inhibitor then was infused in three groups of renovascular hypertensive rats after their blood pressure had been decreased by pretreatment with the converting enzyme inhibitor enalapril (MK 421), saralasin, or sodium nitroprusside, respectively. Infusion of the inhibitor produced an immediate 30% increase in blood pressure only in the enalapril-treated group. These results indicate that bradykinin is involved in the decrease of blood pressure produced by converting enzyme inhibition in experimental renovascular hypertension.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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4. |
Systemic and Renal Vascular Responses to Dietary Calcium and Vitamin D |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 975-982
EDWARD ZAWADA,
JULIE TERWEE,
DANIEL MCCLUNG,
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摘要:
To assess the consequences of hypercalcemia on systemic and renal bemodynamics, vasoactive hormones, and water and electrolyte excretion in intact, conscious mongrel dogs, measurements in 10 dogs receiving 100 mg/kg calcium gluconate and 10,000 U/kg vitamin D daily for 2 weeks were compared with measurements made in 10 tune-control dogs not receiving calcium or vitamin D. Hypercalcemia induced by dietary supplementation with calcium and vitamin D resulted in profoundly reduced glomerular filtration rate (40 vs 78 ml/min in controls;p< 0.005), estimated renal plasma flow (145 vs 267 ml/min in controls;p< 0.005), and renal blood flow (254 vs 441 ml/min in controls;p< 0.005). Renal resistance was significantly increased in the hypercalcemic dogs (0.57 ± 0.07 vs 0.28 ± 0.01 mm Hg/ml/min;p< 0.005). Hypercalcemia also resulted in increased fractional excretion of water (4.8 vs 1.4% in controls;p< 0.005), sodium (1.4 vs 0.6% in controls;p< 0.005), calcium (1.7 vs 0.7% in controls;p< 0.01), and magnesium (10.2 vs 4.1% in controls;p< 0.005). Systolic blood pressure (160 vs 172 mm Hg in controls;p< 0.05) and stroke volume were lower (0.024 vs 0.036 L/beat in controls;p< 0.005) in hypercalcemic dogs, presumably because of the diuresis, while total peripheral resistance was higher (36 vs 31 mm Hg/L/min;p< 0.05) in controls. Magnesium levels were significantly lower in the experimental group (1.3 vs 1.7 mg/dl in controls;p< 0.0005). Aldosterone levels, plasma renin activity, and urinary prostaglandin excretion were not significantly affected. These results suggest that hypercalcemia induced by chronic dietary supplementation increases total peripheral resistance and renal vascular resistance, which may be due to the direct effects of increased calcium ions or to indirect effects on other vasoactive humoral systems including reductions in magnesium ions.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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5. |
Similarities of Essential and Spontaneous Hypertension Volume and Number of Blood Cells |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 983-989
GIACOMO BRUSCHI,
MARILENA MINARI,
MARIA BRUSCHI,
LUISA TACINELLI,
BARBARA MILANI,
ANGELO CAVATORTA,
ALBERICO BORGHETTI,
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摘要:
Spontaneously hypertensive rats have long been used as an animal counterpart of human essential hypertension. The validation of this strain as a model rests mainly on the “clinical” similarity of the two syndromes, but it has scarcely been founded on numerical comparison of measurable parameters. We investigated three hematological indexes previously recognized to be altered in spontaneously hypertensive rats: the single-cell volume of erythrocytes, the single-cell volume of platelets, and the erythrocyte number. Erythrocyte volume was lower by 7%, platelet volume was higher by 12%, and erythrocyte count was higher by 22% in spontaneously hypertensive rats in comparison with Wistar-Kyoto controls. More unexpectedly, it was found that erythrocyte volume is lower by 2%, platelet volume is higher by 3%, and erythrocyte number is higher by 6% in essential hypertensive subjects when compared with normotensive healthy subjects. These results, combined with previously reported blood cell alterations in subjects and rats, reinforce the evidence of a biological similarity between essential and spontaneous hypertension.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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6. |
Potassium Depletion Ameliorates Hypertension in Spontaneously Hypertensive Rats |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 990-996
STUART LINAS,
ROCHELLE MARZEC-CALVERT,
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摘要:
The hemodynamic effect of moderate K+depletion in hypertension is unknown. Since severe K+depletion reduces systemic vascular resistance in normotensive rats, we determined the effect of K+depletion on the natural history of hypertension in spontaneously hypertensive rats (SHR). Wistar-Kyoto rats (WKY) and SHR were fed a K+-replete, a moderately K+-depleted, or a severely K+-depleted diet. After 6 weeks, systemic vascular resistance was reduced by 25% in WKY on the severely K+-depleted diet while mean arterial pressure and systemic vascular resistance were comparable in WKY on the other two diets. In SHR on the severely K+-depleted diet for 6 weeks, muscle K+was reduced by 23% and growth rate by 65%. In SHR on the moderately K+-depleted diet, growth rate was reduced by 23% after 3 weeks. By 6 weeks, however, muscle K+was reduced by 5 to 6% and growth rate was comparable to that in SHR receiving the K+-replete diet. The administration of either K+-depleted diet prevented the development of hypertension (systolic blood pressure: severely depleted, 116 ± 4; moderately depleted, 122 ± 3; K+-replete, 155 ± 5 nun Hg;p< 0.001 compared with both K+-depleted groups) and reversed established hypertension (systolic blood pressure: severely depleted, 116 ± 4; moderately depleted, 128 ± 3; K+-replete, 171 ± 5 mm Hg;p< 0.001 compared with both K+-depleted groups). The protective effect of K+depletion was mediated by a 40% reduction in systemic vascular resistance. These results suggest that K+depletion has a potent antihypertensive effect in SHR. The vasodilative effect of moderate K+depletion also appears to be specific for hypertension since it did not occur in normotensive WKY.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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7. |
Mechanisms by Which Nephrectomy Stimulates Adrenal Renin |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 997-1002
KOREAKI BABA,
YUTAKA DOI,
ROBERTO FRANCO-SAENZ,
PATRICK MULROW,
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摘要:
Renin has been identified in the adrenal gland by several investigators. Nephrectomy is the most potent stimulator of adrenal renin, and in the present study we investigated the mechanism by which nephrectomy stimulates adrenal renin. The pituitary plays a permissive role since hypophysectomy abolished the response of adrenal renin to nephrectomy (from 117.3 ± 14.55 to 10.37 ± 1.63 ng angiotensin I/mg protein/hr) and adrenocorticotropic hormone (ACTH) treatment restored the response to nephrectomy in hypophysectomized rats to 120.26 ± 20.62 ng angiotensin I/mg protein/hr. However, large doses of ACTH given to intact rats did not increase adrenal renin to the high level observed after nephrectomy. Potassium also plays an important role, since prevention of hyperkalemia after nephrectomy by treatment with a cation exchange resin, sodium polystyrene sulfonate (Kayexalate), significantly reduced the adrenal renin response to nephrectomy. A third factor involved is the lack of negative feedback by plasma angiotensin II. Infusion of angiotensin II intraperitoneally prevented the rise in adrenal renin after nephrectomy (from 65.25 ± 7.60 to 9.27 ± 0.99 ng angiotensin I/mg protein/hr) despite an increase in plasma potassium and corticosterone. In conclusion, three factors influence the response of adrenal renin to nephrectomy: 1) the pituitary through the release of ACTH, 2) a direct stimulation by high plasma potassium levels, 3) the lack of angiotensin II feedback inhibition. Whether the high adrenal renin contributes to the high aldosterone observed in rats after nephrectomy remains to be established.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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8. |
Postsynaptic at‐and α2‐Adrenergic Receptors in Adrenergic Control of Capacitance Vessel Tone in Vivo |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 1003-1014
DIETMAR ELSNER,
DUNCAN STEWART,
OLAF SOMMER,
JÜRGEN HOLTZ,
EBERHARD BASSENGE,
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摘要:
The involvement of postsynaptic α2-adrenergic receptors in the adrenergic constriction of the capacitance vessels was studied in anesthetized, spontaneously breathing dogs under ganglionic blockade (hexamethonium, 10 mg/kg + 10 mg/kg/hr; methylatropine, 0.5 mg/kg). Effective vascular compliance was measured as an indicator of venous tone (blood volume was varied by ± 4 ml/kg in an 11-minute cycle of infusion, withdrawal, withdrawal, and reinfusion) and was calculated from the correlation between the observed changes in central venous pressure and the changes in blood volume. Sympathetic activity and central venous pressure were lower and effective vascular compliance was higher than values in untreated conscious dogs. The α2-agonist UK 14,304 (5-bromo-6-[imidazolin-2-ylamino]-quinoxaline; 0.04 and 0.12 μ.g/kg/min;n= 6) dose-dependently lowered compliance and increased central venous pressure to levels found in conscious dogs, as did the ai-agonist methoxamine (10 and 30 μg/kg;n= 6). Rauwolscine (α2-antagonist), 0.3 mg/kg, significantly attenuated the effects of UK 14,304, but not those of methoxamine, while prazosin (α1-antagonist), 0.12 mg/kg, attenuated the effects of methoxamine, but not those of UK 14,304 (n = 6 each). Under β-blockade (nadolol, 2 mg/kg; a = 12) venous tone was increased to about physiological levels by norepinephrine, 0.15 yug/kg/min i.v., or by neuronal norepinephrine release induced by tyramine, 10/ng/kg/min i.v. These increases were significantly attenuated by prazosin as well as by rauwolscine and were abolished by a combination of both. These results indicate that postsynaptic α2-adrenergic receptors (in addition to aradrenergic receptors) are functional in the venous system in vivo and contribute substantially to adrenergic sympathetic and humoral regulation of venous tone.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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9. |
Evidence for a Difference in Vitamin D Metabolism Between Spontaneously Hypertensive and Wistar‐Kyoto Rats |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 1015-1020
THEODORE KURTZ,
ANTHONY PORTALE,
R. MORRIS,
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摘要:
It has been contended that the metabolism of vitamin D in spontaneously hypertensive rats (SHR) is different from that in Wistar-Kyoto rats (WKY). To investigate this possibility, the plasma concentration of 1,25-dihydroxycholecalciferol (1,25[OH]2D) and several known determinants of its production rate were measured in SHR and WKY given normal and restricted amounts of dietary phosphorus. In 12-week-old male SHR given a normal amount of dietary phosphorus, the mean plasma concentration of 1,25(OH)2D (72 ± 5 pg/ml) was significantly lower than that in agematched WKY (129 ± 6 pg/ml;p< 0.001). The lower plasma concentration of 1,25(OH)2D in the SHR could not be attributed to higher circulating levels of inorganic phosphorus or ionized calcium, lower plasma concentrations of 25-hydroxycholecalciferol, or acidosis. However, in the SHR, urinary excretion of cyclic adenosine 3′,5′-monophosphate (12.5 ± 0.4 nmol/mg creatinine) was significantly lower than that in WKY (15.2 ± 0.3 nmol/mg creatinine;p< 0.001). In both SHR and WKY, restriction of dietary phosphorus for 1 week induced an increase in the plasma concentration of 1,25(OH)2D without affecting blood pressure. The current findings Indicate that in 12-week-old male SHR, 1,25(OH)2D metabolism is different from that in age-matched WKY. The activity of 25-hydroxyvitamin D-la-hydroxylase, however, appears to be at least partially responsive to short-term restriction of dietary phosphorus. In SHR, the activity of 25-hydroxyvitamin D-la-hydroxylase may be lower than that hi WKY, perhaps due in part to some impairment in the renal metabolism of, or responsiveness to, cyclic adenosine 3,5′-monophosphate.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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10. |
Salt Level in Weaning Diet Affects Saline Preference and Fluid Intake in Dahl Rats |
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Hypertension,
Volume 8,
Issue 11,
1986,
Page 1021-1026
FAY FERRELL,
AMY LANOU,
SARAH GRAY,
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摘要:
Weanling Dahl salt-sensitive (DS) and salt-resistant (DR) rats were used to compare effects of feeding high or low NaCl diets on taste preference for, and intake of, a wide range of saline concentrations. The DS and DR were fed either 8.0 or 0.4% dietary NaCl for 4 weeks. Then, with all animals fed the 0.4% NaCl diet, their taste preferences for 0.0001 to 0.56 M saline were assessed using three 24-hour two-bottle preference tests of each solution versus distilled deionized water. Saline preference and intake were influenced by concentration and its interaction with genotype, with DS exhibiting higher preferences than DR for hypotonic saline. The DS preexposed to 8.0% dietary NaCl showed elevated consumption levels of water and total fluid (saline + water) that persisted throughout the 5-week test period, despite transfer to the 0.4% NaCl diet before the initiation of preference testing. Findings indicate that genotype, dietary NaCl levels in weaning diet, and saline concentration of preference test solutions interact to influence saline preference and saline and water intake in Dahl rats.
ISSN:0194-911X
出版商:OVID
年代:1986
数据来源: OVID
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