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

We have previously reported an increased urinary excretion of vasopressin without a rise in circulating levels of this hormone in the deoxycorticosterone acetate (DOCA)-hypertensive pig (DH). The present study was designed to characterize the renal handling of vasopressin in DH that might account for this paradox. DOCA hypertension was produced in seven domestic female pigs by means of subcutaneous implants of Silastic rubber impregnated with DOCA. Thirty days after DOCA implantation, urinary clearances of inulin, para-aminohippurate (PAH), and vasopressin were measured in the conscious animals during infusion of a 5% dextrose solution, first without and then with lysine vasopressin. Subsequent to this study, four of the pigs were placed on a low-sodium (10 meq/kg food) diet for 4 wk. At the end of this period, the clearances were again evaluated. We observed an increased urinary vasopressin clearance (CLVP) in the DH associated with an increased urinary flow but without significant changes in the clearances of inulin or PAH. Dietary sodium restrictions reversed the hypertension and the increased urinary flow and returned the CLVP to normotensive levels. These results indicate that the increased urinary excretion of vasopressin in DH is because of an increased urinary clearance of this hormone. This increased urinary CLVP is the consequence of the high urine flow in these pigs.
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PMID:Increased urinary clearance of lysine vasopressin in the deoxycorticosterone acetate-hypertensive pig. 269 Jun 49

To examine right ventricular function during long-term hypoxemia, we instrumented 12 fetal sheep with intravascular catheters and an electromagnetic flow probe on the pulmonary artery. In six cases, hypoxemia was induced by infusing N2 gas into the maternal trachea for 2 wk. Maternal arterial PO2 was less than 60 Torr, and fetal arterial PO2 was reduced from approximately 26 to approximately 19 Torr. Six cases served as nonhypoxic controls. We studied fetal cardiac function by increasing either preload with a volume infusion of 5% (wt/vol) dextrose or afterload by administering methoxamine (alpha-adrenergic agonist). In hypoxic animals, right ventricular output (QRV) and stroke volume (SV) were not affected on the first 2 days but fell 30% on day 3. Fetal arterial pressure (Pfa) increased 20%, hemoglobin concentration increased approximately 30%, and fetal heart rate (FHR) showed minimal changes. Within 2 wk, QRV recovered to normal values, whereas ventricular sensitivity to arterial pressure was reduced. We observed no change in plasma concentration of "cardiac enzymes" or differences in fetal growth between groups. In conclusion, during prolonged hypoxemia, right ventricular function showed a triphasic response (primary maintenance, secondary depression, and subsequent recovery), achieving a new steady state 2 wk after the start of hypoxia, characterized by decreased sensitivity to afterload, associated with polycythemia and hypertension.
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PMID:Cardiac function during long-term hypoxemia in fetal sheep. 276 38

Individuals with cystic fibrosis have a 1% to 7% incidence of insulin-dependent diabetes mellitus. The occurrence of diabetic microangiopathy in patients with cystic fibrosis has been reported recently. From 1978 to 1987, 19 patients with cystic fibrosis and diabetes mellitus were followed up. Four patients (21%) had evidence of diabetic microangiopathy. In one, peripheral neuropathy developed 5 years after the onset of diabetes mellitus, and the other 3 patients each had complications of retinopathy, nephropathy, and neuropathy which developed 10 years after the onset of diabetes mellitus. All were poorly compliant in their medical care. Significant morbidity was seen in the 3 patients with multisystem involvement--blindness, glaucoma, hypertension, and renal failure. The combination of long-standing diabetes mellitus, poor glycemic control, plus pathophysiologic features associated with cystic fibrosis may have contributed to the development of microangiopathy. The use of steroids in 4 other patients and dextrose infusions (as part of hyperalimentation) in another 4 patients precipitated or exacerbated diabetes. The data indicate that diabetic microangiopathy can occur in the individual with cystic fibrosis. Routine screening for diabetes and its complications in the population with cystic fibrosis, as well as optimal control of hyperglycemia, is warranted.
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PMID:Diabetic microangiopathy in patients with cystic fibrosis. 278 Jan 26

The antihypertensive effect and tolerability of enalaprilat, an intravenously administered angiotensin converting enzyme inhibitor, was studied in 65 patients with moderate or severe hypertension. In this randomized, double-blind study, enalaprilat was compared with placebo in 42 (22 enalaprilat, 20 placebo) moderate hypertensive (diastolic blood pressure [BP] 100 to 114 mm Hg) patients. It was compared with furosemide in 23 (12 enalaprilat, 11 furosemide) severe hypertensive (diastolic BP 115 to 130 mm Hg) patients. Enalaprilat (1.25 or 5.0 mg), placebo (5% dextrose) or furosemide (40 or 80 mg) was given every 6 hours intravenously up to 48 hours. In the moderate hypertension stratum, the mean supine diastolic BP was significantly (p less than or equal to 0.01) reduced from baseline at all timepoints in the enalaprilat group. These diastolic BP reductions were significantly (p less than or equal to 0.01) greater in the enalaprilat group than the placebo at 1 to 24 hours (-12 vs -4 mm Hg), with 59% of the patients responding to enalaprilat compared with 30% of the patients responding to placebo. An even greater reduction (p less than or equal to 0.01) was seen at 25 to 48 hours (-14 vs -7 mm Hg, with 73% enalaprilat vs 58% placebo responders). Significant (p less than or equal to 0.01) reductions in mean, supine systolic BP were also seen at 1 to 24 hours (-22 vs -2 mm Hg) and 25 to 48 hours (-24 vs -8 mm Hg) during the 48 hours of the double-blind treatment phase in the enalaprilat group compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of intravenous enalaprilat in moderate and severe systemic hypertension. 284 22

These experiments were designed to assess the interaction of bradykinin and its antagonist (Arg-Pro-Hyp-Gly-Phe-Ser-DPhe-Phe-Arg-trifluoroacetic acid) with the sympathoadrenal system. Three groups of male Wistar rats received 5-minute intra-arterial infusions of either dextrose (Group 1, n = 6), bradykinin, 250 micrograms/min (Group 2, n = 5), or bradykinin, 25 micrograms/min (Group 3, n = 4). Six other groups received a similar infusion of the bradykinin antagonist at 250 micrograms/min. They were either intact rats (Group 4, n = 10) or rats previously submitted to chemical sympathectomy (Group 5, n = 17), to adrenal enucleation (Group 6, n = 8), to combined alpha-adrenergic and beta-adrenergic blockade (Group 7, n = 7), to alpha 1-adrenergic receptor blockade (Group 8, n = 8), or to alpha 2-adrenergic receptor blockade (Group 9, n = 8). Bradykinin infusion produced a sustained fall in mean arterial pressure (MAP) in Groups 2 and 3 (by -48 +/- 3 and -36 +/- 7 mm Hg, respectively) associated with similar increases in plasma epinephrine levels (100-fold), and norepinephrine (sevenfold) as compared with Group 1. The bradykinin antagonist infusion in intact rats produced a 23 +/- 4 mm Hg rise in MAP associated with a sixfold increase in epinephrine and a twofold increase in norepinephrine. Group 5 rats with lower baseline catecholamine levels had an even larger MAP rise (30 +/- 6 mm Hg) accompanied by a rise in epinephrine and norepinephrine proportionally similar to that of intact animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Jun
PMID:Vascular and sympathoadrenal responses to bradykinin and a bradykinin analogue. 289 59

In a double blind, crossover study 6 h infusions of adrenaline (15 ng/kg/min; 1 ng = 5.458 pmol), noradrenaline (30 ng/kg/min; 1 ng = 5.911 pmol), and a 5% dextrose solution (5.4 ml/h), were given to ten healthy volunteers in random order 2 weeks apart. By means of intra-arterial ambulatory monitoring the haemodynamic effects were followed for 18 h after the infusions were stopped. Adrenaline, but not noradrenaline, caused a delayed and protracted pressor effect. Over the total postinfusion period systolic and diastolic arterial pressure were 6 (SEM 2)% and 7 (2)%, respectively, higher than after dextrose infusion (ANOVA, p less than 0.001). Thus, "stress" levels of adrenaline (230 pg/ml) for 6 h cause a delayed and protracted pressor effect. These findings are strong support for the adrenaline-hypertension hypothesis in man.
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PMID:Support for adrenaline-hypertension hypothesis: 18 hour pressor effect after 6 hours adrenaline infusion. 256 20

The present study was designed to investigate the effect of vasoactive agents on cellular proliferation in serially passed cultured vascular smooth muscle cells (VSMC). A substantial reduction in the number of vascular smooth muscle cells was observed with the addition of nifedipine, nicorandil, bunazocine and labetalol compared with that in a control sample. Furthermore, noradrenaline significantly increased the number of vascular smooth muscle cells. In contrast, neither propranolol nor captopril had any effect on number of vascular smooth muscle cells. The cell size, measured as water volume of vascular smooth muscle cells based on the equilibrium distribution of 3-O-(14C-methyl)-D-glucose, did not differ between treatments with the above-mentioned agents. It is suggested that in addition to a known calcium-mediated mechanism, an alpha-receptor-mediated property could be involved in the proliferation of vascular smooth muscle cells and that clinical use of a calcium antagonist or an alpha-blocker might be useful to prevent the hyperproliferation of vascular smooth muscle cells commonly seen in the vascular walls of patients with hypertension.
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PMID:The effects of vasoactive agents on the proliferation of vascular smooth muscle cells grown in vitro. 297 59

We investigated the blood pressure response elicited by microinjection of various hypertonic solutions into the area of the nucleus tractus solitarii (NTS) of the brainstem, an area rich in catecholaminergic neurons. Equiosmolar solutions of NaCl, dextrose, LiCl and KCl were employed. NaCl produced a prolonged blood pressure rise; LiCl and normal saline produced a similar rise of short duration; and KCl produced epileptic-type seizures with postictal hypertension. Dextrose had no effect and neither had NaCl microinjection in areas relatively distant from the NTS. The rise in blood pressure was not reversed by a vasopressin antagonist injected systemically, but was totally abolished by systemic alpha-adrenergic blockade with phentolamine. These findings suggest that sodium can cause hypertension by direct stimulation of the central sympathetic nervous system without participation of peripheral mechanisms such as fluid volume expansion or alteration of the vascular wall.
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PMID:Hypertensive response to saline microinjection in the area of the nucleus tractus solitarii of the rat. 299 26

The effect on blood pressure (BP) of acute and chronic suppression of angiotensin (ANG) II was studied in the two-kidney, one clip hypertensive rat. Conscious, chronically catheterized rats were given a bolus injection of captopril (2.5 mg/kg) followed by a chronic infusion of either dextrose or captopril (1 mg/kg per h) lasting 5 days. Blood pressure was measured continuously by a computer technique. Following the acute injection of captopril, arterial BP fell from 165.1 +/- 19.4 mmHg (mean +/- s.d.) to a minimum of 137.6 +/- 23.3 mmHg after 15 min. Twelve hours after starting the chronic infusion of captopril, BP fell to a minimum of 112.5 +/- 19.4 mmHg. This was significantly lower than that after the acute injection of captopril. Blood pressure remained lower throughout the 5-day infusion ranging, on the 5th day, from 122.1 +/- 23.4 to 136.0 +/- 30.2 mmHg. In contrast, BP continued to rise in rats given dextrose chronically ranging, on the 5th day, from 163.6 +/- 23.8 to 180.4 +/- 22.5 mmHg. Both the fall in pressure after acute captopril and that after chronic captopril were related to pre-treatment levels of plasma renin concentration. These results suggest that in the two-kidney, one clip hypertensive rat ANG II, in addition to its acute vasoconstrictor property, contribute to the hypertension through a secondary effect, the mechanism of which is as yet uncertain.
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PMID:Effect of acute and chronic captopril infusion on blood pressure in the two-kidney, one clip hypertensive rat. 300 90

Because kidney microangiopathy with capillary basement membrane thickening has been reported in spontaneous hypertension, we have studied the activities of three lysosomal glycosidases able to degrade the carbohydrate moieties of basement membrane constituents in the kidney cortex of 12-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar Kyoto rats (WKY). These activities were also determined in SHR and WKY treated from 6 to 12 weeks of age with hydralazine (mean dose, 18 mg/kg per day in drinking water). Sialidase specific activity on sialyl-alpha 2-3-[3H]lactitol was markedly decreased in the kidney of untreated SHR, 40% activity remaining relative to that found in untreated age-matched WKY (p less than 0.001). beta-Galactosidase specific activity on p-nitrophenyl-beta-D-galactoside was also decreased, 86% activity remaining relative to that found in untreated WKY (p less than 0.001). Glucosyl-galactosyl-hydroxylysyl glucohydrolase specific activity on glucosyl-galactosyl-hydroxylysine was equally diminished, 74% activity remaining relative to that found in untreated age-matched WKY (p less than 0.001). In contrast, the activities of two control glycosidases inactive on the carbohydrate moieties of basement membrane constituents, alpha-glucosidase assayed with p-nitrophenyl-alpha-D-glucoside as substrate and beta-glucosidase assayed with p-nitrophenyl-beta-D-glucoside as substrate, were significantly increased. All the alterations in enzyme activities observed in the kidney of SHR were also present in the long-term treated normotensive SHR. No effect of the hydralazine treatment on the three enzyme activities investigated could be demonstrated in the WKY. Thus the alterations observed in the kidneys of SHR appear to be independent of blood pressure level.
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PMID:Alteration in sialidase and other glycosidase activities in the kidney of spontaneously hypertensive rats: persistence after preventive treatment with hydralazine. 321 99


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