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

Sodium and calcium contents of cardiovascular tissue in spontaneously hypertensive rats (SHR) and DOCA hypertensive rats were investigated. The effect of salt loading on these contents of SHR and control Wistar rats was also investigated. Calcium content increased with the development of hypertension, but not sodium content particularly in salt loading rats and at the sustained stage of DOCA hypertensive rats. These results suggest that calcium rather than sodium is more intimately related to the increase in blood pressure.
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PMID:Studies on sodium and calcium contents of cardiovascular tissue in experimental hypertension. 83 30

1 The role of monoamine oxidase (MAO) in the maintenance of deoxycorticosterone-sodium chloride (DOCA-salt) hypertension was investigated by assaying the MAO activity both in central as well as peripheral blood vessels and in brain tissue. 2 The results suggest that the activity of MAO in the DOCA-salt hypertensive rat is similar to the activity present in the normotensive rat.
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PMID:Brain and vascular monoamine oxidase activity in the deoxycorticosterone-salt hypertensive rat. 84 81

D,L-Propranolol given in single doses by gavage or s.c. injection to awake rats, always slowed the heart without affecting blood pressure. Doses of 0.2 mg/100 g injected twice daily lowered systolic pressure after 3 days in DOCA hypertensive but not in normotensive or spontaneously hypertensive rats. When chronic treatment with propranolol preceded the induction of DOCA hypertension, the pressure elevation attained 14 weeks later was less in treated than in untreated rats. Pressor responses to injected norepinephrine and to posterior hypothalamic stimulation were significantly larger in DOCA hypertensive rats that had been treated chronically with propranolol than in those that had not. These results suggest that propranolol's antihypertensive effects are unimpressive because they are simultaneously opposed by an enhanced cardiovascular responsiveness to pressor stimuli.
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PMID:Propranolol in DOCA hypertensive rats: development of hypertension inhibited and pressor responsiveness enhanced. 88 Sep 80

Prevention of high blood pressure in uninephrectomized, DOCA-saline treated rats was observed after treatment with central tyramine precursors. We suggest that the high blood pressure is either due to relative lack of tyrosine, which might be caused by the hyperactivity of tyrosine hydroxylase, or to hypoactivity of the decarboxylase: in both cases the result is diminished tyramine synthesis.
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PMID:Central tyramine prevents hypertension in uninephrectomized DOCA-saline treated rats. 92 98

Labelled proline incorporation into collagenous and noncollagenous proteins of aorta or mesenteric arteries was significantly increased in 70-day-old spontaneously hypertensive rats (SHR) at the early stage of hypertension in comparison with normotensive Wistar-Kyoto (WK) rats; however such an increase was not detected in 30-day-old SHR at the prehypertensive stage. Similar increases in the proline incorporation were noted in 70-day-old renal hypertensive rats and in DOCA hypertensive rats in which hypertension had been induced similarly to that om SHR. Furthermore, the decay of the specific activity of noncollagenous and collagenous proteins was studied for 100 days after labelled proline infusion. The dacay of the noncollagenous protein activity was clearly accelerated in the heart, aorta and especially in the mesenteric arteries of SHR compared with WK. The decrease in the hydroxyproline radioactivity of the collagenous protein was significantly faster in the aorta and mesenteric arteries in SHR. These results proved the increased protein metabolism in the arterial walls in the relatively early stage of hypertension in SHR as well as in experimental hypertension, and then suggested its importance in the common pathogenetic mechanisms of hypertension.
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PMID:Vascular protein metabolism in the pathogenesis of hypertension. 96 68

Several methods were used in an attempt to produce preeclampsia in the pregnant rat. Desoxycorticosterone acetate plus increased NaCl intake produced hypertension, proteinuria, rapid weight gain, convulsions, decreased litter size, decreased offspring weight, increased fetal and maternal mortality, and renal lesions similar to those seen in human preeclampsia. Injection of placenta in Freund's adjuvant produced mild blood pressure elevation and proteinuria in the pregnant rat. Rabbit antirat placenta serum produced hypertension in the pregnant rat but not in the nonpregnant rat. Liver congestion and renal glomerular congestion were observed in both pregnant and non-pregnant rats. Pregnancy in the rat reduced hypertension produced by applying a Goldblatt clamp prior to breeding. Uterine ischemia produced by wrapping the uterus in cellophane produced mild blood pressure elevation and proteinuria. A vitamin-E-deficient diet that contained substantial amounts of partially perioxidized, polyunsaturated fatty acids produced morphological lesions in the pregnant rat similar to those seen in human preeclampsia, but hypertension, edema, and proteinuria were absent. None of the maneuvers was effective in producing a complete model of human preeclampsia, but they do provide material for study that could answer somebasic questions about preeclampsia.
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PMID:The rat as a model for preeclampsia. 100 52

The realtionship between in vitro prostaglandin production by renal medullary tissue and hypertension was investigated in three models of hypertensive rat, i.e., DOCA, Goldblatt and SHR. Medullary minces were incubated for 30 minutes. Following incubation tissue PGE2 concentration was quantified using mass fragmentography. Media PGE2 concentrations were quantified using radioimmunoassay. Concentrations of PGE2 in tissue from Goldblatts and SHRs were significantly less than normotensive controls. The concentration of PGE2 in media after incubating SHR tissue was significantly less than normotensives. The data suggest that alterations in PGE2 metabolism are similar in Goldblatt and SHR hypertension.
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PMID:Prostaglandin E2 production by renomedullary tissue of DOCA, Goldblatt and spontaneously hypertensive rats. 100 18

The permeability of the vascular wall to the penetration into it of fibrinogen and serum protein in experimental hypertension of rats (ischemic renal and corticosteroid hypertension) was studied. Use was made of the indirect variant of Coons' method involving application of antisera to the mouse fibrinogen and to serum protein of rats. The development of the study models of experimental hypertension in rats was accompanied by an elevated vascular permeability and insudation of the plasma into the vasal wall. The disruption of the vascular permeability was more pronounced in arterioled of different organs of rats with DOCA-saline hypertension.
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PMID:[Vascular plasmorrhagia in experimental hypertension]. 102 21

1. The arteriolar lesions of rats with deoxycorticosterone (DOCA)-salt hypertension have been studied by colloidal carbon injection and light- and electron-microscopy. 2. Colloidal carbon particles enter the media of arterioles to form focal deposits when hypertension develops. 3. The focal lesions are similar to those seen after angiotensin infusion or renal artery constriction. They are characterized by endothelial damage and plasma deposition in the media. 4. Heavy deposition of carbon in the glomeruli of DOCA-treated animals was found to be caused by increased mesangial uptake and not by hypertensive vascular damage. 5. Angiotensin II concentrations fell during the development of hypertension and vascular lesions. The renin-angiotensin system was not implicated in the development of vascular damage in this form of hypertension.
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PMID:The arteriolar lesions of steroid hypertension in rats. 107 33

Electrical stimulation of the posterior hypothalamus is followed by an immediate increase in sympathetic nerve activity and rise in blood pressure. Destruction of hypothalamic adrenergic structures by local unilateral injection of 6-hydroxydopamine into the posterior hypothalamus reduced the blood pressure rise in response to stimulation of the lesioned side. This and numerous other findings indicate an involvement of central adrenergic neurons in the mediation of an increase of sympathetic nerve activity caused by hypothalamic stimulation. However, central adrenergic neurons do not seem to be an integral part of the sympathoexcitatory pathways originating in the posterior hypothalamus but rather facilitate their activation: after almost complete norepinephrine depletion produced by combined treatment with reserpine and alpha-methl-p-tyrosine, hypothalamic stimulation was still followed by an increase in spontaneous sympathetic nerve activity. Stimulation of an alpha-adrenoceptive site, probably located in the lower brain stem, mimics an activation of the baroreceptor reflex. The hypotensive drug, clonidine, stimulates this alpha-adrenoceptive site. In low doses clonidine facilitates the activation of the reflex, and in high doses this drug induces a state which closely resembles a pronounced activation of the reflex. Experiments following depletion of norepinephrine suggest that the central part of the baroreceptor reflex arc does not contain adrenergic neurons. However, these findings are compatible with the view that some neurons within the reflex arc are supplied with alpha-adrenoceptors. For the present it cannot be stated with certainty whether these alpha-adrenoceptors possess an innervation by adrenergic neurons projecting onto the reflex arc. In favor of such an innervation are the obsevations that alpha-methyldopa has its site of action in the lower brain stem and that the integrity of central adrenergic neurons is essential for its hypotensive effect. It seems that two central adrenergic systems exist with opposing effects on cardiovascular control. These are an excitatory hypothalamic and an inhibitory bulbar adrenergic system. Partial destruction of central adrenergic neurons by intraventricularly injected 6-hydroxydopamine prevents the development of DOCA/NaCl, renal, and neurogenic hypertension and alters the pattern of blood pressure rise in spontaneously hypertensive rats. Impairment of central adrenergic function or imbalance of the two central adrenergic mechanisms may represent a trigger mechanism for the initiation of hypertension.
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PMID:Cardiovascular regulation by central adrenergic mechanisms and its alteration by hypotensive drugs. 109 54


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