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

The fawn-hooded rat (FH rat) develops hypertension accompanied with focal and segmental glomerulosclerosis and proteinuria, resulting in premature death. In a first experiment the relationship between renal lesions and blood pressure at various ages was investigated. In a second experiment blood pressure was measured weekly from 10 to 38 weeks of age in a number of male FH rats, followed by examination of renal tissues at 40 weeks of age. Plasma renin activity (PRA) had also been determined in individual FH rats. FH rats aged 4.5 weeks had no renal morphological abnormalities. The severity of the glomerulosclerosis increased with age and showed a positive relationship with blood pressure. The scores of the proteinaceous tubular casts also increased with age and they, too, showed a positive correlation with blood pressure. The severity of glomerulosclerosis and proteinaceous casts at 40 weeks of age was related positively to the course of blood pressure throughout life. The final blood pressure level showed a positive correlation with final PRA values. Only FH rats with malignant nephrosclerosis had high PRA values. The renal glomerular and vascular lesions in the FH rat, most likely caused by the hypertension, progressively deteriorate to malignant nephrosclerosis. At that stage PRA values are increased and may be contributing to the development of renal vascular lesions and acceleration of the hypertension.
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PMID:Relationship between blood pressure level, renal histopathological lesions and plasma renin activity in fawn-hooded rats. 355 93

Smooth muscle cell (SMC) growth may play an important role in the pathogenesis of vascular diseases such as atherosclerosis and hypertension. Recent studies have demonstrated that, under different growth stimuli in vivo, SMC may respond by proliferation of diploid cells, polyploidization to the tetraploid (or even octaploid) state, or both. In this study, we used flow cytometry to evaluate the intrinsic tendencies of aortic SMC and nonarterial cells from rats of different strains, ages, and blood pressures to polyploidize in response to in vitro growth stimulation. Significant strain-related differences in polyploidization of aortic SMC were found (P less than 0.001): highest in WKY (normotensive inbred rat related to SHR), intermediate in SHR (genetically hypertensive rat), and lowest in Sprague-Dawley and Fischer (normotensive outbred and inbred rats). Animal age had less or no effect on the degree of polyploidization. Nonarterial cells (venous SMC and lung cells) from WKY and SHR remained essentially diploid, suggesting tissue specificity of in vitro polyploidization. Studies of the growth kinetics of uncloned and clonal populations of aortic SMC revealed decreased proliferation as the ploidy increased in WKY, SHR, and Sprague-Dawley. These findings suggest that genetic strain factors as well as cell type/site of origin significantly influence in vitro polyploidization, whereas animal age and blood pressure do not. The findings also emphasize the need to consider ploidy changes when evaluating in vitro SMC growth kinetics. Further studies will improve understanding of SMC growth regulation and the functional significance of vascular polyploidy.
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PMID:Strain and site dependence of polyploidization of cultured rat smooth muscle. 373 93

Rats were exposed to alcohol vapor for 6 days and the mean blood ethanol concentration (BEC) was obtained for each subject. Blood pressure and its reactivity to noradrenaline and a thromboxane-mimic U46619 were directly measured on day 6 via a catheter implanted in the tail artery of normal and ethanol-treated animals. The mean BEC for each subject correlated with mean arterial blood pressure (MAP); an increase in BEC was associated with a decrease in MAP (p less than 0.02). The mean MAP of subjects with BEC less than 168 mg% was 8% higher than normal (not significant), whereas, the mean MAP of subjects with BEC greater than 182 mg% decreased 27 +/- 4% (p less than 0.01). Conversely, the pressor response to U46619 was markedly enhanced (p less than 0.005) in rats with mean BEC greater than 182 mg% at all doses investigated (12.5-3200 ng per rat). Increases in the pressor response to noradrenaline in ethanol-treated rats were significant only when maximally stimulated by 400 and 800 ng doses (p less than 0.03). A 3-fold increase in sensitivity for U46619 was seen in subjects with high mean BEC, however, sensitivity for noradrenaline did not significantly change. Vasoreactivity was not effected in rats with mean BEC less than 168 mg%. These data demonstrate that a moderate mean BEC for 6 days induces a tendency towards a mild hypertension, whereas, high mean BEC induces marked hypotension which is associated with hyperreactivity. Long-term exposure to high blood ethanol concentrations may predispose the alcohol-dependent rats to hypertensive disease and vasospastic disorders, at least partially, as a result of enhanced sensitivity to prostaglandins such as thromboxane.
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PMID:The effect of chronic alcohol inhalation on blood pressure and the pressor response to noradrenaline and the thromboxane-mimic U46619. 376 8

Conscious SHR and WKY rats were infused during 7 days with synthetic ANF (Arg 101-Tyr 126), 100 ng/hr/rat (35 pmol/hr/rat) by means of miniosmotic pumps. The SHR initial blood pressure of 177 +/- 5 mmHg gradually dropped to 133 +/- 3 and 142 +/- 4 mmHg the last two days of infusion. No significant change in blood pressure was observed in the ANF-infused WKY group. No apparent difference in natriuresis or diuresis was observed in ANF-infused SHR and WKY when compared with non-infused control groups. A slight but significant lower immunoreactive ANF concentration was found in the atria of SHR than in their normotensive controls. No difference in cardiac weight was found between infused and non-infused rats. It is suggested that the hypotensive response observed in SHR and not in WKY is due to a decrease in vascular peripheral resistance. Whether ANF is involved in the development and maintenance of high blood pressure in SHR remains to be elucidated.
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PMID:Chronic infusion of low doses of atrial natriuretic factor (ANF Arg 101-Tyr 126) reduces blood pressure in conscious SHR without apparent changes in sodium excretion. 400 Nov 34

A "bolus" dose (110 microgram) of the angiotesin II (A II)-blocker 1-Sar-8-Ala-A II (Saralasin, S) followed by its slow rate infusion (5 microgram/min/rat) for thirty min, was injected before and after the complete ganglionic blockade by pentolinium (P) in unanaesthetized unilaterally clipped renal hypertensive rats (the opposite kidney remained untouched). Pentolinium was also injected like a "bolus" dose (3 mg) followed by slow infusion (0.1 mg/min/rat) for thirty min. The observations were made until the fifth week after clipping the left renal artery. A consistent maximal hypotensive response was observed after the "bolus test" with both drugs. When S was the first drug injected, an inverse correlation was found between the percent decrease in arterial pressure (BP) by S and the percent decrease in BP by P (r = --0.83, P < 0.01, n = 8). Thus whenever a greater hypotensive effect was obtained by S, a smaller neural pressor component remained to be blocked by P. On the other hand, when P was the first drug injected a lesser A II pressor component remained to be blocked by S in the hypertensive rats. The results suggest that a considerable A II pressor effect in two-kidney renovascular hypertension is mediated via neurogenic mechanisms from the first week. A direct pressor vasoconstriction was found to be significant in cases with very high plasma-renin activity.
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PMID:Humoral and neurogenic factors in two-kidney renovascular hypertension. 615 37

Widespread arteriosclerotic lesions were detected by histological examinations of rats killed at seven or nine weeks after an intrarenal (ir) injection of nickel subsulfide (Ni3S2, 5 mg per rat). Arteriosclerotic plaques were readily visualized by administering hematoporphyrin derivative (HPD) iv to rats at 24 hours before sacrifice. At necropsy, the major arteries were inspected under ultraviolet light, revealing patches of intense HPD-fluorescence in the arterial endothelium of Ni3S2-treated rats, but not in control rats. Consistent with previous reports, the Ni3S2-treated rats developed pronounced erythrocytosis; blood hematocrit values averaged 70 +/- 4 percent at seven weeks after ir injection of Ni3S2 (P less than 0.001 vs corresponding value of 49 +/- 2 percent in vehicle controls). At seven weeks, blood platelet counts averaged 17 percent lower and serum glucose concentrations averaged 23 percent lower in Ni3S2-treated rats than in controls; serum lipids, lipoproteins, non-protein nitrogen constituents, electrolytes, proteins, and enzymes were not significantly affected. Body weights and systolic blood pressures of rats at two, four, and six weeks after ir injection of Ni3S2 did not differ from corresponding values in controls. Addition of egg yolk to the diet caused mild hypercholesterolemia, but it did not enhance the incidence or severity of arterial lesions in Ni3S2-treated rats. These findings exclude hypertension and hyperlipidemia as pathogenic factors in Ni3S2-induced arteriosclerosis.
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PMID:Studies of the pathogenesis of arteriosclerosis induced in rats by intrarenal injection of a carcinogen, nickel subsulfide. 623 39

Myocardial hypertrophy, with high morbidity and mortality, is a natural outcome of hypertensive heart disease. The increase in myocardial mass is associated with a cellular and subcellular reorganization of the myocytes. The following study uses rapid myothermal techniques to assess the contribution of the major intracellular changes to the adaptive hypertrophic process in various heart models. Pressure overload and thyrotoxic hypertrophy were produced in the rabbit. In the rat, hypertrophy was produced by constricting the renal artery (Goldblatt hypertensive rat) or by using the spontaneously hypertensive rat strain. Atrophy was produced by administration of propylthiouracil in the drinking water. The V1/V3 myosin isoenzyme ratio was decreased in the pressure overload, Goldblatt, and propylthiouracil animals. This was associated with a decrease in total activity-related heat, initial heat, and tension-dependent heat per tension time integral. The tension-independent heat was decreased in the pressure overload, while the time to peak tension was increased. The economy of the metabolic recovery process was unchanged in the pressure overload and Goldblatt preparations. In the propylthiouracil preparation the recovery processes became uneconomical. The spontaneously hypertensive rat exhibited mild cardiac hypertrophy but in all other respects the heart was unchanged from the normal animals. The thyrotoxic hearts had a high V1/V3 myosin isoenzyme ratio, which was associated with a high total activity-related heat, initial heat, and tension-dependent heat per tension time integral. The tension-independent heat was reduced in the thyrotoxic preparations. The appropriateness of each of the intracellular changes is evaluated in terms of the demands made on the heart.
Hypertension
PMID:The inhomogeneity and appropriateness of the myocardial response to stress. 624 Apr 54

Contractile responses to norepinephrine (NE) of strips of vasa deferentia from prostatic end isolated from rats with genetic hypertension and deoxycorticosterone (DOC)-salt induced hypertension were examined. Maximum responses to NE of vasa deferentia from all hypertensive and corresponding normotensive control rats were biphasic. Spontaneous rhythmic activities superimposed on the NE-induced contraction were observed in most of the SHR (spontaneously hypertensive rat) strips, some of the WKY (Wistar-Kyoto normotensive rat) strips and none of the NWR (regular normotensive Wistar rat) strips. Neither the fast- nor the slow-component of the maximum contractile response to NE was altered in the vasa deferentia from SHR compared to those from WKY and in vasa deferentia from DOC-salt hypertensive rats (DHR) compared to those from the corresponding DOC-salt treated but normotensive controls (DNR). However, the strips from NWR developed significantly greater tension than those from WKY and DNR. Our findings suggest that interpretation of studies on hypertension in rats should take into account differences between tissues related to the strain of the rats used as controls for genetic hypertension.
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PMID:On the abnormalities of contractile responses of rat vasa deferentia to norepinephrine in genetic hypertension. 646 42

The effects of centrally administered neuropeptide Y (NPY) on the sleep-wakefulness cycle have been studied by analyzing its action in different strains of rats with or without spontaneous hypertension and during two different phases of the circadian cycle. Normal adult Sprague-Dawley (SD), Wistar-Kyoto (WKy) and spontaneous hypertensive (SH) rats were used. By means of EEG electrodes the recording of the fronto-parietal electrocorticogram and the electromyogram could be made. Stainless steel cannula were also implanted into the lateral ventricle. The effects of an intraventricular injection of NPY (1.25 nmol/rat) was compared with the effects of the vehicle (saline) alone. The EEG patterns were classified as desynchronized, mixed or synchronized. In the SD rats NPY produced behavioural signs of sedation and a significant reduction of synchronized EEG activity as well as significant increase of synchronized and mixed EEG activities in comparison with the saline treated rats. In the WKy rats NPY administration produced an increase of synchronized EEG activity during evening sessions. In SH rats NPY produced a significant increase of desynchronized EEG activity and a decrease in mixed EEG activity indicating an awakening effect of the peptide. In view of the NPY innervation of the locus ceruleus, it therefore seems possible that the neuronal and hormonal regulation of the locus ceruleus noradrenaline nerve cells is different in the two strains of rats. It also seems possible that the ability of NPY to increase wakefulness in hypertensive animals is related to abnormal changes in the alpha 2-adrenoreceptors taking place in SH rats.
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PMID:Actions of centrally administered neuropeptide Y on EEG activity in different rat strains and in different phases of their circadian cycle. 654 58

Infusions of carbachol into the posterior region of the 3rd ventricle of rats for 7 days produced a sustained elevation of blood pressure and heart rate at doses of 0.6 and 1.2 microgram/hr, but only transient rises in blood pressure were obtained at 2.4 microgram/hr. Carbachol, at 0.6 microgram/hr, increased water consumption. At 1.2 microgram/hr, the dipsogenic effect was observed in 50% of the animals and at 2.4 microgram/hr there was no significant change in drinking. Plasma vasopressin levels, measured by radioimmunoassay, were increased by 19-fold 3 min after acute i.c.v. administration of carbachol (0.5 microgram/rat). However, in rats infused with carbachol for 2 or 5 days, the vasopressin levels were not significantly different from controls. The pressor responses to acute and chronic administration of carbachol could be ascribed to the stimulation of periventricular muscarinic receptors because the effects were blocked by atropine, but not by hexamethonium. In carbachol-infused animals, the pressor responsiveness to i.v. norepinephrine and vasopressin were unchanged. From studies using phentolamine, chlorisondamine and a specific vasopressin vasopressor antagonist, it could be inferred that the pressor responses to acute i.c.v. injections of carbachol were due to increased sympathetic activity and vasopressin release. However, the sustained hypertension produced by chronic infusion of carbachol was due primarily to increased sympathetic activity and not to increased plasma levels of vasopressin.
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PMID:Mechanisms underlying the pressor responses to acute and chronic intraventricular administration of carbachol in the rat. 669 15


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