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

Renal functional reserve (renal response to protein loading, RFR) has been suggested as a method to verify the presence of hyperfiltration. This study was designed to evaluate the role of RFR as an indicator of increased glomerular capillary hydrostatic pressure in short-term treated and untreated rats with two-kidney, one-clip Goldblatt hypertension. One month after placing a silver clip, micropuncture studies were performed on the unclipped kidney. Normal rats and three groups of clipped rats [untreated group (HYP), a group treated with captopril (CEI) and a group treated with verapamil (VER) 5 days before the micropuncture studies] were studied. Glomerular hemodynamics and proximal tubular reabsorption were measured in control period and during intravenous administration of glycine (G). In normal rats, G produced afferent and efferent dilation, increases in single nephron plasma flow (SNPF) and single nephron glomerular filtration rate (SNGFR) of 24%. Systemic hypertension in HYP rats was associated with increases in transcapillary pressure gradient (delta P) and SNGFR. In this hyperfiltration state, infusion of G did not modify SNGFR of SNPF defining loss of RFR. The antihypertensive treatment was equally effective in normalizing MAP and delta P in CEI and VER, but only CEI rats responded to G with a 20% increase in SNGFR due to an increase in delta P. The most striking findings were that loss of RFR in both HYP and VER rats was associated with a significant decrease in absolute and proximal fractional reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal functional reserve in treated and untreated hypertensive rats. 178 41

Management of epistaxis is directly related to the site of the bleeding. Anterior nosebleeds are the least dangerous and the most common, especially among children. Sinus disease, colds, allergies, abrupt temperature changes and dry heat produce fragile and hyperemic nasal mucosa that bleeds easily with nose blowing or mild abrasion. Anterior epistaxis can be reached easily and stopped by pinching the nostrils, applying silver nitrate cautery or lightly packing the anterior nose. Posterior epistaxis may be severe and may be more difficult to locate and control. Occurring more often in the elderly, posterior nosebleeds are frequently associated with hypertension, atherosclerosis and conditions that decrease platelets and clotting function. Visualization of the bleeding site is enhanced by proper positioning of the patient, use of topical vasoconstricting anesthesia and suctioning. Anterior and posterior nasal packing, hospitalization, antibiotics and close follow-up may be required to control posterior nosebleeds.
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PMID:Management of anterior and posterior epistaxis. 204 44

Cerebral vasospasm occurs, following subarachnoid haemorrhage, in the majority of patients and is accompanied by cerebral ischaemia in 30%. The objectives of this article are to review (1) the effects of subarachnoid haemorrhage and vasospasm on cerebral blood flow (CBF); (2) the effects of induced hypotension and hypocapnia on CBF in these patients; (3) current therapy for cerebral ischaemia from vasospasm. The medical literature was searched using Index Medicus; for the period 1983-90 this search was done on a computer with the CD-ROM version of Index Medicus, Silver Platter. Papers were selected on the basis of validity and applicability to clinical practice; animal studies are included when human data is lacking. Cerebral vasospasm may decrease cerebral blood flow, disturb autoregulation and place the patient at risk for delayed cerebral ischaemia. Intraoperative induced hypotension and hypocapnia can decrease CBF further, although effects of either on outcome have not been evaluated. Calcium antagonists are effective for both the prevention and the treatment of delayed cerebral ischaemia. Of the mechanical treatments, systemic-arterial hypertension has the firmest scientific foundation, although this is frequently combined with haemodilution and blood volume expansion. There is a need for randomized clinical trials to assess the efficacy of these latter treatments.
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PMID:Haemodynamic considerations in the management of patients with subarachnoid haemorrhage. 206 13

STUDY OBJECTIVE - The aim was to examine the contractile state, the inotropic response to [Ca2+]e and the Ca2+ sensitivity of the contractile proteins in different models of hypertensive hypertrophy in an early stage of evolution (3-4 weeks). DESIGN - Renal hypertension was induced by placing a silver clip around the left renal artery. The contralateral kidney was either removed (1K-1C) or left untouched (2K-1C). Hypertension through sodium overload was produced by administration of deoxycorticosterone and 1% NaCl drinking water. (DOCA rats). Active and passive length-tension curves were performed to evaluate basal contractility at Lmax and passive stiffness of cardiac muscle. The inotropic responsiveness to [Ca2+]e and the Ca2+ sensitivity of the contractile proteins were also evaluated. EXPERIMENTAL MATERIAL - Papillary muscles and skinned trabeculae from the left ventricle of male Wistar hypertensive and age matched normotensive rats were used. MEASUREMENTS AND RESULTS - Cardiac hypertrophy was similar in all hypertensive groups. In 2K-1C and 1K-1C rats, basal contractility was not significantly different from controls. In DOCA rats, developed tension and time to peak tension (TTP) were significantly greater than controls. The inotropic response to [Ca2+]e was depressed in 2K-1C and increased in DOCA rats. In DOCA rats, increasing [Ca2+]e produced an increase in TTP greater than in controls. No differences were detected in muscle passive stiffness or in Ca2+ sensitivity of the contractility proteins among the different groups. CONCLUSIONS - In the earlier stages of hypertensive hypertrophy, differences in basal contractile state and/or inotropic responsiveness appear to be more related to the initiating cause of hypertensive hypertrophy than to the degree of hypertrophy itself. These differences cannot be attributed to changes in Ca2+ sensitivity of the contractile system.
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PMID:Calcium sensitivity of isometric tension in intact papillary muscles and chemically skinned trabeculae in different models of hypertensive hypertrophy. 214 71

Previous studies from our laboratory, have demonstrated that 21 days after unclipping the decrease in arterial pressure (AP) was followed by a regression of cardiac hypertrophy (CH) and a normalization of contractile response to Isoproterenol (I) stimulation in two kidney one clip (2K1C) hypertension. The purpose in this study was to reexamine the effects of Alpha Methyl Dopa (AMD) treatment on AP, CH and cardiac response to I stimulation in this model. A total of 43 male rats, ten weeks old, were used. In 19 rats a silver clip was placed under ether anaesthesia in the left renal artery (clip group) (K). The remaining 24 animals constituted the control group (C). Twenty one days later, in 9 and in 17 animals from K and C groups, treatment with AMD 100 mg/kg/day per os was started and maintained during the three week-follow-up period (K alpha and C alpha groups). AP was measured twice a week by the tail cuff method and body weight was registered once a week. We defined hypertension when the systolic pressure was 150 mmHg or more. Three weeks after clipping and 21 days after treatment, in the clipped animals, simultaneously with matched controls (C alpha and K alpha) the cardiac response to Isoproterenol stimulation was studied. For this purpose, under pentobarbital anesthesia the carotid artery and the femoral artery and vein were cannulated in order to measure mean arterial pressure (MAP), left ventricular systolic pressure, heart rate (HR) and DP/DT+ Max in basal conditions and after I (0.001, 0.02, 0.04, 0.12 and 0.24 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of alpha methyldopa on heart in renovascular hypertension]. 215 63

Neuropeptide Y is known to enhance blood pressure responsiveness to various constrictors, including angiotensin II, and to suppress renin secretion. This study was undertaken to assess the effect of neuropeptide Y on the development of two-kidney, one clip renal hypertension. Normotensive rats either had a silver clip placed on the left renal artery or were sham-operated upon. An osmotic minipump, which was connected via a catheter to a jugular vein, was implanted subcutaneously in all rats. These pumps delivered either neuropeptide Y (0.001 microgram/min) or saline intravenously. Eight days later, an intra-arterial catheter was inserted and the rats were studied while not anesthetized on the following day. Neuropeptide Y did not affect body weight. In clipped rats, neuropeptide Y prevented the development of hypertension and suppressed renin secretion. Neuropeptide Y significantly decreased blood pressure also in sham-operated rats, although it had no effect on plasma renin activity. These data indicate that prolonged neuropeptide Y infusion may lower blood pressure by different mechanisms, one of which is probably a suppression of renin release.
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PMID:Prevention of renal hypertension in the rat by neuropeptide Y. 215 52

The participation of the central serotonergic system in the development of two-kidney, two clip (2K2C) Goldblatt renovascular hypertension in the rat has been examined. Half of the rats were treated with desmethylimipramine intraperitoneally and 5,7-dihydroxytryptamine intracisternally; the other half received only desmethylimipramine and the 5,7-dihydroxytryptamine vehicle. Two days later, a silver clip was placed in both renal arteries in half of the rats of each group. A sham operation was performed in the remaining rats. Blood pressure was recorded during the 5 weeks after treatment. At the end of the experiment, blood and cerebrospinal fluid samples were obtained. The brain was dissected into several areas and kept frozen. Norepinephrine, serotonin, angiotensinogen, and renin-like concentration were evaluated in the brain areas. Plasma renin activity and angiotensinogen concentration in the plasma and cerebrospinal fluid were estimated. In the sham-operated groups, blood pressure was lower in the treated than in the control rats. The curve of blood pressure increase, as well as the final blood pressure, was similar in the treated and control 2K2C rats. Serotonin was significantly depleted by the 5,7-dihydroxytryptamine treatment in all brain areas. Treatment did not induce any changes in central norepinephrine concentration. Plasma renin activity was diminished in the treated sham-operated rats. These data indicate that the central serotonin depletion does not prevent the development of hypertension and confirm the role of the amine in normal blood pressure regulation. On the other hand, the peripheral renin-angiotensin system might participate in the development of high blood pressure in serotonin-depleted animals.
Hypertension 1990 Feb
PMID:Development of renovascular hypertension after central serotonin depletion. 240 59

The effect of ketanserin (Kt) has been analyzed during the development of two-kidney-two-clip (2k-2c) renovascular hypertension in the rat. Male Wistar rats were divided into four experimental groups: (1) clip Kt (ClKt) (n = 12)--A silver clip (0.25 mm width) was placed in each renal artery 3 days after beginning the administration of Kt (10 mg/kg/day) in the drinking water; (2) sham Kt (ShKt) (n = 13)--Similar to group 1, but the clips were placed in, and immediately removed from, the renal arteries; (3) untreated clip (UCl) (n = 10)--Similar to group 1, but the rats drank water; (4) untreated sham (USh) (n = 10)--Similar to group 2, but the rats drank water. Blood pressure (BP) was measured before surgery and was followed weekly for 7 weeks. At the end of this period, blood and cerebrospinal fluid (CSF) samples were obtained in all the animals. Plasma renin activity (PRA) and plasma and CSF angiotensinogen concentration (AoC) were evaluated. The results have shown that Kt partially inhibited the increase in BP induced by bilateral renal ischemia (BP: UCl rats 180.5 +/- 12.4 versus ClKt rats 149.8 +/- 5.1 mm Hg; p less than 0.01; USh rats 116.7 +/- 3.7; ShKt rats 114.4 +/- 5.0 mm Hg). PRA was similar in hypertensive and control rats whether or not they had received Kt. AoC in plasma was decreased in clipped treated and untreated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic administration of ketanserin and the development of two-kidney-two-clip Goldblatt renovascular hypertension in the rat. 244 74

The present experiment was performed in order to evaluate some of the actions of ketanserin, a blocking agent active at the serotonin 2 (S2) receptors. Male rats were divided into: 1. Two kidney-two clip (2K-2C) renal hypertensive: a silver clip (0.25 mm width) was placed in both renal arteries. 2. Sham-operated: a similar operation without placing the clip was performed. Blood pressure (BP), heart rate and pressor responses to tyramine, angiotensin II and norepinephrine (NE), and the hypotensive effect of prazosin (Pz) and ketanserin (Kt) were recorded in the conscious animals 8 weeks later. Results showed that Pz produced a similar decrease in BP in hypertensive and sham animals while Kt lowered BP much more in hypertensive than in normotensive rats. Prazosin abolished the pressor response to tyramine while ketanserin only diminished tyramine effect. Both hypotensive agents shifted the dose-response curve to NE to the right. Present data have shown that ketanserin and prazosin are effective hypotensive agents in 2K - 2C renovascular hypertension in the rat. They also suggest that both hypotensive compounds have an alpha 1-blocking effect, somehow they seem to have some differences in their pattern of pharmacological action.
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PMID:Effect of ketanserin and prazosin on blood pressure and cardiovascular reactivity to vasopressor agents during the development of two kidney-two clip renal hypertension in the conscious rat. 247 91

Three operated cases of lobar intracerebral hemorrhage (LICH) related to cerebral amyloid angiopathy (CAA) were studied clinicopathologically. They constituted about 8% of all LICH cases (n = 37) operated upon in our institute (DUSM) during the past 3 years. Case 1, 2 and 3 aged 71, 67 and 73 years, respectively. There were 2 males (Cases 1 & 2) and 1 female (Case 3). Only one case (Case 3) had both hypertension and dementia before hemorrhage. In all 3 cases, neurologic symptoms deteriorated after admission. The hematoma involved the right temporo-parietal in 1 (Case 1), the right parieto-occipital in 1 (Case 2) and the left fronto-parietal region in 1 (Case 3). Case 1 developed a new hematoma in the right occipital lobe on the day following surgery. On CT, the hematoma was multilobular in shape and located very superficially extending to the subarachnoid space in all cases. There was no abnormal enhancement in and around the hematoma upon contrast infusion. Angiography showed only an avascular mass sign in case. At surgery, the hematoma was extruded onto the cortical surface in all cases. The surgical outcome was good in 2 (Cases 1 & 2) and fair in 1 (Case 3). Removed hematomas, solid nodular tissues and adjacent brain tissues were examined histologically using hematoxylin and eosin, Azan-Mallory, elastica van Gieson, silver and Congo red stains. Arteries in the hematoma wall, the subarachnoid space and the adjacent brain parenchyma were intensely stained with Congo red and showed birefringence on polarized light.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lobar intracerebral hemorrhage secondary to cerebral amyloid angiopathy: a clinicopathologic study of three operated cases]. 269 77


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