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

A simple technique is described for producing severe reproducible renal hypertension in the rat. Total ligation of the aorta between the renal arteries and just below the origin of the superior mesenteric artery resulted in sustained systolic and diastolic pressures in 90 per cent of 170 rats studied. Arterial pressure is then measured in the conscious unrestrained rat through a carotid cannula inserted no more than 48 hours before measurements are made. The mean arterial pressure increases to a peak of 180 mm. Hg at day 5 and then remains at a plateau of 160 mm. Hg through the 40 days of the study. Plasma renin increases to a peak at 5 days but returns to baseline at 30 days despite the persistence of severe hypertension. Infarction of the left kidney below the aortic constriction results in no increase in pressure or plasma renin. Infarctions of the right kidney by emboli originating from the indwelling carotid cannula are associated with greater increases in blood pressure and plasma renin than the standard preparation. Prolonged carotid cannulation must be avoided in order to prevent such emboli. This simple technique for producing renal hypertension allows studies on the pathogenesis of hypertension with an excellent degree of reproducibility and reliability.
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PMID:Experimental model of severe renal hypertension. 77 2

Utilizing the microsurgical method of transplantation in the rat, the role of the kidney in an experimental renal hypertension due to segmental renal infarction was studied. When the infarcted kidney was transplanted into the bilaterally nephrectomized recipient, hypertension developed so long as the donor kidney was transplanted within 2 weeks after infarction. With transplantation of the normal kidney into the hypertensive rat 8 weeks after infarction, BP remained high unless the infarcted kidney was removed. PRA after transplantation, or KRA of the transplanted kidneys were not correlated to the blood pressure levels. It was suggested that the infarcted kidney has the pressor mechanism, lasting for 2 weeks or more after infarction. The infarcted kidney also has the maintenance mechanism, establishing 8 weeks after infarction.
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PMID:Role of the kidney in the development and maintenance of hypertension caused by renal segmental infarction in the rat. 79 91

In about 15% of cases hypertension is caused by renal diseases, including unilateral and bilateral parenchymatous nephropathies, renal artery stenosis and renin producing tumors. Important pathogenic determinants are the sodium volume status and the renin angiotensin system. The level of the blood pressure may also depend on the duration of hypertension. An increase in peripheral resistance plays a more important role than an increase in cardiac index. Simultaneous determination of the renin activity in both renal veins is of decisive importance in the diagnosis of renal artery stenosis. Drug treatment of renal hypertension is not essentially different from that of essential hypertension. Surgical procedures include revascularization, uninephrectomy and, in uncontrollable hemodialysis patients, binephrectomy.
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PMID:[Renal hypertension]. 79 75

Late onset (3-7 yrs) post-transplant renal hypertension is usually an indication of chronic, irreversible renal damage, and is a poor prognostic sign. In a small percent of patients (10%) however, hypertension can persist for years in conjunction with excellent renal function, and the absence of any known causes of early or late hypertension. This primary hypertension does not seem related to the recipient's pre-transplant blood pressure nor to the original renal disease. Rather, the high incidence of essential hypertension in the respective living related donor suggests that either a hypertensive diathesis exists, common to donor and recipient, or a transplantable factor inherent to the graft, or both causes, predispose to late onset primary hypertension.
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PMID:Late hypertension in renal transplant recipients: possible role of the donor in late primary hypertension. 80 Oct 58

To study the extent and time course of arterial baroreceptor threshold resetting to increases in blood pressure, renal hypertension was induced in young normotensive male Wistar rats by unilateral renal artery constriction. At different intervals after operation the extent of baroreceptor threshold resetting in the carotid sinus was examined. Experiments were performed 7, 14 and 25 days after renal artery clipping to enable baroreceptor resetting to be correlated with the rate and extent of cardiovascular changes in rats which had renovascular hypertension of indentical durations (Lundgren et al. 1974). Baroreceptor thresholds in the carotid sinuses were established by progressive clamping of both carotid arteries after partial vascular isolation of the sinuses. The results show that after one week of hypertension baroreceptor resetting is only just apparent but by two weeks resetting is gross and seems to be largely completed. This parallels the adaptive changes in the hindquarters of renal hypertensive rats and it is concluded that baroreceptor resetting is a secondary phenomenon related to the structural changes induced in the vessels by the elevated blood pressure.
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PMID:Time course and extent of carotid sinus baroreceptor threshold resetting in rats with renovascular hypertension. 84 74

1. We describe a new method of producing two-kidney hypertension in dogs by a two-step procedure with complete occlusion of a renal artery 2 weeks after it was partially constricted. 2. Control mean arterial pressure (96 +/- 3 mmHg) of nine conscious, trained dogs rose to 107 +/- 3 mmHg 2 weeks after partial constriction of a renal artery, and it stabilized at a sustained hypertensive plateau (124 +/- 7 mmHg) 3 weeks after complete occlusion. 3. Intravenous infusion of an angiotensin II antagonist (Sar1-Thr8-angiotensin II) caused arterial pressure to fall during the acute but not the chronic phase of renal hypertension. In this latter phase plasma renin activity had returned to control values. 4. We conclude that the renin-angiotensin system appears not to be directly involved in the chronic phase of two-kidney hypertension in the dog.
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PMID:The course of arterial pressure and the effect of Sar1-Thr8-angiotensin II in a new model of two-kidney hypertension in conscious dogs. 84 49

In a Zurich outpatient clinic in 1975 hypertension was found in 10.4% of 8228 patients (3657 females and 4571 males). Essential (primary) hypertension was found in 92.9% of all hypertensives. Among secondary forms of hypertension (7.1%) renal hypertension was the most common (5.8%) with 4.9% for hypertension of renal parenchymatous origin, .8% renovascular hypertension, and .1% hypertension associated with unilateral hydronephrosis. In 2 patients (.2%) the underlying disease was primary aldosteronism and in 5 (.6%) coarctation of the aorta. In 4 females (.5%) hypertension was caused by oral contraceptives. Patients with essential hypertension had higher body weight than those with normal blood pressure. These differences were statistically significant in young and middle-aged patients. The percentage of primary hypertension was significantly high. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone-producing adenoma of the adrenal gland, and oral contraceptives). The very low percentage of curable forms of high blood pressure should be kept in mind when deciding on expensive procedures in a search for secondary forms of high blood pressure.
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PMID:[Primary and secondary hypertension in polyclinical patients]. 85 17

Properties of the longitudinal smooth muscle of portal veins from normotensive Wistar rats, adult (NCR) and young (NCRy); spontaneously hypertensive Okamoto rats, adult (SHR) and young (SHRy); and adult Wistar rats with renal hypertension (RHR) were studied in vitro and histologically. Some aortic strips from SHR and SHRy were compared with controls. In response to noradrenaline (NA) and acetylcholine (ACh) greater maximum force was developed by veins from all hypertensive groups than by those from control rats. Cross-sectional area of the longitudinal muscle of veins from SHR but nor SHRy nor RHR was greater than control. Maximum stress in response to agonists was greater in both SHR and RHR than NCR. ED50-values for NA and ACh were lower in portal veins from SHR than NCR but not from RHR nor SHRy compared to controls. Denervation did not abolish any of the differences between SHR and NCR. Aortic strips from SHR developed less maximum force to NA and ED50 was greater than those from NCR, i.e. opposite to the findings in portal veins. Low levels of external Ca2+ reveal altered calcium handling in veins from SHR compared to controls. It is concluded that portal veins from hypertensive rats are functionally different from those of normotensive rats and differ in SHR compared to RHR. It is suggested that the altered functional properties of portal vein, but not of aorta, in several respects resemble those of arterial resistance vessels. The implications of these findings are discussed in terms of mechanisms of hypertension in these animal models.
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PMID:Contractility, muscle mass and agonist sensitivity of isolated portal veins from normo- and hypertensive rats. 85 13

Several reports have suggested that a central action of the renin-angiotensin system plays a role in the development of renal hypertension. Based on the identification of the anteroventral thrid ventricle (AV3V) as a site of central angiotensin dipsogenic and pressor mechanisms, the present study examined the effect of electrolytic lesions in the AV3V region on the development of renal hypertension in rats. Lesioning alone produced a temporary but profound adipsia and, in one-half of the rats, a substantial transient elevation in arterial pressure. After lesioned rats had recovered normal drinking and blood pressure, unilateral nephrectomy with figure-of-eight wrapping of the remaining kidney failed to produce the hypertension and increased drinking observed after renal wrapping in shamlesioned rats. The possibility that the failure of lesioned rats to increase water intake after wrapping prevents hypertension development was ruled out by experiments demonstrating that normal rats exhibited identical rises in arterial pressure after wrapping regardless of whether or not they were allowed to increase water intake. The fact that unanesthetized lesioned rats exhibit attenuated drinking and pressor responses to systemically administered angiotensin suggests this mechanism as a possible explanation for the failure of AVV-lesioned rats to increase drinking and blood pressure after renal wrapping.
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PMID:Prevention of the development of renal hypertension by anteroventral third ventricular tissue lesions. 85 73

The response of the intima-media of the thoracic aorta to 1 to 4 weeks of two-kidney renal hypertension in the rat has been analyzed by morphometric techniques at light and electron microscopic levels. The increased thickness of the aorta that ensues is the result of an increase in the size but not the number of smooth muscle cell layers. The volume fractions of intima occupied by endothelium (26%), internal elastic lamina (37%), and subendothelial space (37%) in normotensive animals are not significantly altered by the hypertension. The percent increases in muscle cross-sectional area is greatest (58 to 60%) in the two innermost layers (M1 and M2). M1 is composed of nearly equal compartments of smooth muscle cells and interstitial space that expand 69% and 50%, respectively, with hypertension. Analysis of the subcellular constituents of the M1 smooth muscle cells indicates that significant changes in absolute volume include increases of caveolae (45%), myofibrils (59%), mitochondria (81%), glycogen (163%), and rough endoplasmic reticulum (221%). Factors contributing to these alterations are discussed.
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PMID:Morphometric analysis of hypertension-induced hypertrophy of rat thoracic aorta. 88 10


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