Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old male with "pure" progressive autonomic failure ("pure" PAF) was admitted to our hospital in June 1988, with a chief complaint of recent syncopal attacks while standing. Since the age of 35. He has noticed dyshidrosis on his left side. The family history was negative. Neurological examination showed dyshidrosis on his left side and profound orthostatic hypertension. No other neurological abnormalities were noted. Autonomic function tests revealed sympathetic and parasympathetic dysfunction as follows: Adrenaline administered subcutaneously gave a hyperactive pressor response from 136/82 mmHg to 190/116 mmHg with the pulse increasing from 54 to 150 beats per min. Hidrosis was observed on the right side of the body in response to heat. However, it was observed over the whole body in response to pilocarpine. In the studies of pupillary response to instillation of 1.25% epinephrine, both pupils were unchanged in diameter; after 5.0% tyramine, both pupils were dilated from 3.5 mm to 5.0; and after 2.5% methacholine, the right and left pupils, each originally 4.5mm were constricted to 3.5 mm and 4.0 mm, respectively. From the above data, this case was diagnosed as "pure" PAF. 133Xe inhalation method. The mean regional CBF (F1) values were reduced from 91 to 53 ml/100 g brain/min by postural change from supine to sitting position, associated with a decrease in mean arterial blood pressure (MABP) of 28 mmHg (from 103 to 75 mmHg). This result shows the impairment of CBF autoregulation in this patient. This case adds further evidence to the hypothesis that the autonomic nervous system plays a role in CBF autoregulation.
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PMID:[A case of "pure" progressive autonomic failure with impairment of cerebral blood flow autoregulation]. 269 14

Atenolol is a newer betablocker, widely used as an antihypertensive drug. It cause a large and rapid fall in IOP when used orally and topically. A total of 33 patients both having normal and raised IOP were included in the study. The drug was given in a dose of 50 mg. tab. orally once a day for 7 days at 8 A.M. and IOP recorded after 24 hours, 72 hours and on 7th day. It produces significant and sustained fall in IOP in both normal and raised IOP patients besides lowering of systematic B.P. and pulse rate. The IOP on patients with systemic hypertension with Atenolol will be reduced and stoppage of therapy may cause glaucoma damage.
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PMID:A clinical study of effect of oral atenolol on normal intraocular pressure and systemic blood pressure. 270 Apr 74

1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure. 5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation. 6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.
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PMID:Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits. 271 53

To investigate the potential role of sympathetic nerves in preventing pronounced increases in cerebral blood flow, we evaluated the effects of abrupt hypertension on the cerebral circulation of newborn pigs with intact cerebral sympathetic innervation and after cerebral sympathetic denervation. Epinephrine infusion was used to induce abrupt increases in mean (+/- SEM) arterial pressure (innervated pigs, 62 +/- 3 mm of Hg to 115 +/- 3 mm of Hg; denervated pigs, 71 +/- 4 mm of Hg to 132 +/- 4 mm of Hg) that remained increased for the 3 minutes of the study. Abrupt hypertension increased blood flow to all brain regions. In denervated pigs, the increased flow to the cerebrum was prolonged, compared with that in pigs with intact sympathetic innervation. Differences between pigs of the innervated and denervated groups were not apparent, with respect to blood flow to any other region (caudate region, brain stem, cerebellum). In newborn pigs, sympathetic nerves may attenuate hypertension-induced increases in blood flow to the cerebrum, but do not appear to affect flow to the rest of the brain.
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PMID:Effects of hypertension and sympathetic denervation on cerebral blood flow in newborn pigs. 272 21

Clinical use of the immunosuppressant cyclosporine A (CyA) is associated with nephrotoxicity and hypertension of unknown mechanisms. Because the vascular endothelium is now known to influence vascular tone by release of relaxing factors and CyA can damage endothelial cells, it was of interest to determine if CyA could induce a rise in blood pressure (BP) in normal rats and if this was associated with increased vascular responses to constrictor stimuli and/or decreased responses to endothelium-dependent dilators. Male Wistar rats were treated daily for 21 days by gavage with 5, 10 or 20 mg/kg of CyA or olive oil vehicle (1 ml/kg). Creatinine clearance was measured before treatment and on day 19. On day 20 the rats were anesthetized with ether and a carotid artery cannulated and exteriorized. On day 21 mean arterial BP and heart rate were recorded directly for 1 hr while the rats were conscious and unrestrained. An arterial blood sample was taken for analysis of catecholamines by high-performance liquid chromatography. The rats were then anesthetized and both kidneys isolated and perfused at 3 ml/min with Krebs' solution. Vasoconstrictor responses were obtained to periarterial renal nerve stimulation (1-30 Hz) and to bolus injections of norepinephrine (10-300 ng), angiotensin II (1-30 ng) and potassium (30-100 mumol). Perfusion pressure was then increased by 125 mm Hg with a norepinephrine infusion and vasodilator responses obtained to the incremental infusion of acetylcholine (1 nM-1 microM) and nitroprusside (100 nM-3 microM). CyA treatment decreased creatinine clearance and produced a dose-dependent increase in BP and heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporine treatment of normal rats produces a rise in blood pressure and decreased renal vascular responses to nerve stimulation, vasoconstrictors and endothelium-dependent dilators. 278 81

A 47-year-old female presented with hypertension, hypokalaemia, low plasma renin, high plasma aldosterone and was found to have a left adrenal tumour 4 cm in diameter by computerized tomography. Detailed biochemical studies showed high plasma levels of 11-deoxycorticosterone and corticosterone in addition to aldosterone and 18-hydroxycorticosterone. Basal 11-deoxycorticosterone levels were particularly high. Corticosterone, 18-hydroxycorticosterone and aldosterone concentrations were abnormally sensitive to infusions of ACTH and angiotensin II. Plasma cortisol and assays for sex hormones were normal although there was evidence that cortisol derived from the neoplasm. At operation a well-differentiated adrenocortical carcinoma weighing 50 g (56 X 30 X 36 mm) was removed. There was no evidence of metastases following surgery. Adrenal function returned to normal. Review of the literature suggests that adrenocortical carcinoma should be suspected in patients who otherwise have typical features of Conn's syndrome, but whose tumours are more than 3 cm in diameter. Measurement of steroids such as 11-deoxycorticosterone in addition to aldosterone is recommended since abnormally high values may also help to distinguish between hyperaldosteronism due to adenoma and carcinoma. Previously reported cases of isolated aldosterone production by a carcinoma cannot be substantiated.
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PMID:Hypermineralocorticoidism due to adrenal carcinoma: plasma corticosteroids and their response to ACTH and angiotensin II. 282 95

beta 2-Adrenoceptors on lymphocytes from healthy nonpregnant and pregnant women and patients with pregnancy-induced hypertension (PIH) were studied in vitro by a radioligand binding technique (125I-hydroxybenzylpindolol) and related to in vivo responses to infused adrenaline. Healthy pregnant women had significantly fewer beta 2-adrenoceptor binding sites than nonpregnant controls (47.1 +/- 5.6 vs. 73.6 +/- 10.5 fmol X mg-1 protein), PIH patients displaying intermediate values. Adrenaline-induced increases in plasma cyclic AMP (a beta 2-mediated in vivo response) also tended to be reduced during normal pregnancy. The systemic vasodilatation evoked by intravenously infused adrenaline and the density of lymphocyte beta 2-adrenoceptor binding sites were positively related in the nonpregnant controls (r = 0.50), but inversely related in both the pregnant controls (r = -0.40) and the PIH patients (r = -0.70). These regression lines differed significantly. The present results indicate a reduction of beta 2-adrenoceptor function during normal pregnancy, which is less pronounced in PIH, as well as an altered relationship between beta 2-mediated vasodilator responses and densities of beta 2-adrenoceptors on lymphocytes during pregnancy.
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PMID:Reduced beta 2-adrenoceptor sensitivity in normal pregnancy but not in pregnancy-induced hypertension. 284 Dec 7

The effects of daily, intraperitoneal injections of LiCl (3 mEq/kg) on systolic blood pressure (SBP) and adrenal catecholamine levels were measured in spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKY). Control animals from each strain were injected with equivalent volumes (0.1 ml/100 g b.wt.) of 0.9% saline (0.15 mEq/kg). SBP in LiCl-treated SHR was significantly lower (p less than 0.05) than that of saline-treated SHR (177 +/- 7 vs. 196 +/- 4 mm Hg, respectively) after one week. After two weeks SBP was lower in LiCl SHR than in saline controls, but this difference was not significant. While SBP of both LiCl and saline treated WKY was not significantly different (146 +/- 4 vs. 147 +/- 8 mm Hg, respectively), SBP in both WKY groups remained lower than the SBP for either group of SHR. LiCl induced a significant weight loss in the SHR, but not in the WKY. Adrenal norepinephrine and epinephrine were significantly (p less than 0.05) higher in LiCl-treated rats of both strains; dopamine was also higher in LiCl-treated rats of both strains, but significant only between SHR-LiCl and SHR controls. It appears that LiCl's effect in slowing the development of hypertension is independent of its action on adrenal catecholamines. The SHR's increased sensitivity to LiCl, relative to weight loss and SBP, may reflect differences in genetic or physiological status of the animal compared to WKY. These differences may be associated with alterations in membrane ion transport systems.
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PMID:Lithium chloride stabilizes systolic blood pressure and increases adrenal catecholamines in the spontaneously hypertensive rat. 285 79

A retrospective follow-up study of 206 eyes with exfoliation in 164 patients was carried out. At the time exfoliation (EX) was initially diagnosed, there were 97 patients with unilateral and 42 patients (84 eyes) with bilateral exfoliation. In 25 patients the exfoliation was connected with hypertension or glaucoma in the fellow eye. The average age of the patients with unilateral EX was 66.3 years and that of the patients with bilateral EX 68.0 years. The initial mean IOP (+/- SD) of 17.9 (+/- 2.9) mmHg in 97 unilateral EX eyes was statistically significantly higher (2p less than 0.001) than in the normal fellow eye 16.1 (+/- 2.5) mmHg. Of the 97 eyes with unilateral EX, 45.3% with an initial mean IOP of 17.4 mmHg remained unchanged. The mean follow-up time was 5.0 years. Conversion of unilateral to bilateral EX was observed in 14.4% of cases. The mean time of conversion was 4.5 years. Of the 84 bilateral EX eyes with an initial mean IOP of 17.0 mmHg, 66.7% remained unchanged. Of the total sample of 206 EX eyes, 65.5% remained normotensive and 34.5% developed hypertension or glaucoma during the follow-up period. The initial mean IOP of those eyes which remained normotensive was statistically significantly lower than that of those which later on developed hypertension or glaucoma (2p less than 0.001).
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PMID:Intraocular pressure in exfoliation syndrome. 285 21

The purpose of the present study was to analyse the mechanisms of the vasodepressive action of diltiazem (one of the Ca antagonists) in hypertension. The perfused mesenteric preparation was used in spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-9 weeks old) and age-matched Wistar-Kyoto rats (WKY). The effects of diltiazem on norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were investigated. Pressor responses to electrical nerve stimulation were inhibited dose-dependently by diltiazem. Norepinephrine overflow during periarterial nerve stimulation was also inhibited by diltiazem, and its suppression was significantly greater in SHR than in the age-matched WKY rats. Vasoconstrictor responses to exogenous norepinephrine were also reduced by diltiazem in both SHR and WKY rats. The inhibitory effects of diltiazem were more evident in SHR than in WKY rats. These results demonstrate that diltiazem could affect both pre- and postsynaptic sites of the resistance vessels and cause a decrease in electrically stimulated norepinephrine overflow from the sympathetic nerve endings, in addition to the direct effects on the responsiveness of the vascular smooth muscles. The marked reduction of the pressor responses and norepinephrine overflow by diltiazem in SHR might explain the Ca-dependency in the pathogenesis of hypertension.
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PMID:Effects of diltiazem (a calcium antagonist) on neurosecretion and vascular responsiveness in hypertension. 285 97


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