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

On intravenous injection into cats, lysophosphatidic acid elicited a biphasic change in arterial blood pressure: sharp hypotension followed immediately by hypertension. Respiration was greatly disturbed immediately after injection of lysophosphatidic acid, and remained stimulated for a long period, and the heart rate increased during the period of hypertension. Unsaturated lysophosphatidic acids were more potent in evoking hypertension than saturated ones. The hypotensive activity of 1-palmitoyl-2-0-acetyl-sn-glycero-3-phosphate was about half that of 1-palmitoyl-2-lyso-sn-glycero-3-phosphate (lysophosphatidic acid). Elongation of the acyl chain at the sn-2-position of the glycerol moiety resulted in progressive reduction in the hypotensive activity. Chemically modified analogs with a head group, such as phosphoryl-methanol, ethanol, propanol and choline, had little or no activity. However, sn-2-acetyl-analogs of lyso-phosphatidyl cholines had hypotensive activity. 1-0-Hexadecyl-2-lyso-sn-glycero-3-phosphate, an alkyl-lyso-phosphatidic acid, had much stronger hypotensive activity than the corresponding acyl-lysophosphatidic acid, like its sn-2-0-acetyl analog. These structure-activity relationships of lysophosphatidic acids indicate the existence of their specific binding sites on cardiovascular cells.
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PMID:Effects of lysophosphatidic acids and their structural analogs on arterial blood pressure of cats. 384 54

The vasoconstrictor and vasopressor actions of vasopressin have been revealed in recent research through the use of highly specific and sensitive radioimmunoassays, employment of peptide antagonists, and comparison with an animal model which has hereditary absence of this hormone, the Brattleboro rat. Factors now known to modify the pressor effect of vasopressin are the baroreflexes, local vascular prostaglandin production, and a specific interaction with angiotensin II. In experimental models the volume retaining, but not the vasoconstrictor effect of vasopressin is necessary for mineralocorticoid-salt hypertension. Vasopressin contributes directly to the increase in arterial pressure of glycerol induced acute renal failure. In nephrectomized rats, plasma vasopressin is elevated and contributes directly to maintenance of pressure. Vasopressin antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension and in one genetic model, spontaneously hypertensive rat (SHR), but the peptide is not necessary for hypertension in these models. Plasma vasopressin is reduced in primary aldosteronism, but may be elevated in malignant hypertension. In essential hypertension, there is considerable disagreement among various studies in which plasma vasopressin, urine vasopressin excretion, platelet associated vasopressin, or vasopressin-neurophysin were measured as to whether there is evidence for increased secretion of vasopressin. Only preliminary studies of vasopressin antagonism in clinical hypertension have been reported. At present, there is no conclusive evidence that elevated vasopressin secretion occurs or is necessary for any form of clinical hypertension.
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PMID:The role of vasopressin in experimental and clinical hypertension. 388 2

The health consequences of obesity in adults encompass both metabolic and cardiovascular complications. Pregnancy in obese women also has a particular set of problems. For the obese pregnant woman, these include weight gain less than 5.4 kg, chronic hypertension and superimposed preeclampsia, gestational diabetes, multiple gestation, and the potential for a macrosomic child. The combination of obesity and maternal diabetes does not appear to have an additive effect on the excessive growth of infants of obese mothers. Furthermore, despite inadequate weight gain, hypertension, and multiple gestation, infants of obese mothers are usually born with a greater birth weight than those of nonobese women. In addition, the incidence of intrauterine growth retardation is lower after an obese pregnancy. Neonates born to obese mothers have increased risk for birth asphyxia and birth trauma. Recently infants born to obese women were noted to have transient neonatal fasting asymptomatic hypoglycemia. Hyperinsulinism is not present in the infants of obese mothers; thus, alternate fuel mobilization (free fatty acids, glycerol, ketones) may respond to the hypoglycemic stimulus. Suggestions and rationale for the management of the pregnant obese woman, fetus, and newly born infant are discussed in the text.
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PMID:Perinatal problems of the obese mother and her infant. 389 77

Twenty nine patients with trigeminal neuralgia were treated by retrogasserian glycerol injection method. Two of 29 were postherpetic and 27 were idiopathic trigeminal neuralgia. The mean age of these 27 was 65.2 years old ranging from 35 to 83 and the mean duration of symptoms was 7.6 years ranging from 6 months to 25 years. As previous surgical treatment there were 9 alcohol block, 5 thermorhizotomy of the Gasserian ganglion and one microvascular decompression. Twenty-two gauge needle was introduced into the trigeminal cistern via foramen ovale under the fluoroscopic control. Before injection of glycerol trigeminal cisternography using metrizamide of 300 mgI/dl was done to ascertain whether or not the needle tip was properly placed in the cistern. Patients' neck being flexed anteriorly, pure glycerol, amounting from 0.15 to 0.6 ml, was injected into the cistern with small increments through the needle. If the needle was inserted too deeply in the cistern, it is more probable that glycerol should escape from the cistern into the posterior fossa. So it was advisable that needle tip should be placed in the bottom of the cistern. When there was no pain relief, second injection was performed usually 7 days after the first injection. Complications were as follows; dysesthesia (81%), hypertension (70%), hypalgesia and hypesthesia (48%) headache (22%), ocular dysesthesia (11%), masseter weakness (7%), hyperalgesia (7%), attack of paroxysmal pain (7%). Most of these complications subsided within 8 weeks. Dysesthesia and hypalgesia that had persisted over 8 weeks were recognized in 30% of the cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Glycerol injection method for trigeminal neuralgia]. 401 Aug 77

The available evidence indicates that nitrendipine and other dihydropyridines with a similar pharmacological action exert their therapeutic effects by inhibiting Ca2+ channels. In our recent experiments, nitrendipine was shown to block K+-stimulated 45Ca2+ uptake and K+-induced contractions of isolated rabbit aortic rings. Its IC50 were 4.7 and 8.9 nM for inhibition of Ca2+ uptake and of contractions, respectively. There was no statistically significant difference between the two values. At higher concentrations, nitrendipine also reduced norepinephrine-induced 45Ca2+ uptake and norepinephrine-induced contractions of rabbit aortic strips. The norepinephrine-induced contractions were only slightly (21%) reduced by nitrendipine at 10 microM. Nitrendipine at 10 nM and higher concentrations inhibited K+- or angiotensin-II-(AII) induced release of aldosterone from isolated bovine adrenal glomerulosa cells. The drug was more potent and more effective in inhibiting K+- than AII-induced aldosterone release. Dantrolene, 25 microM, enhanced the inhibitory activity of nitrendipine on AII-stimulated aldosterone release. Acute renal failure produced by either glycerol or gentamicin in rats was antagonized by nitrendipine at oral doses of 15-25 mg/kg/day. Our studies confirmed previously reported observations that the usefulness of nitrendipine in the treatment of hypertension may be determined not only by its vasodilator action. We demonstrated that nitrendipine has a direct inhibitory effect on the release of aldosterone from adrenal glomerular cells. In addition to a previously described diuretic action, nitrendipine was shown to have renal cytoprotective activity.
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PMID:Some recent pharmacological findings with nitrendipine. 608 81

Injection of lysophosphatidic acid into anesthetized rats induced immediate hypertension, the effect depending on the structure of the sn-1-acyl moiety of the molecule. A hydroxyl group at the sn-2-position was not necessary, but a wedgeshaped structure was suitable for hypertensive activity. Most lysophospholipids with a chemical group attached to the phosphate portion had only weak hypotensive effects, but the sn-2-acetylated analogs of these depressor lysophospholipids elicited a hypotension at much lower doses. The durations of the hypotensions evoked by the sn-2-acetylated choline phospholipids were longer than those produced by 1-palmitoyl-2-acetoyl-sn-glycerol-3-phosphorylmethanol, ethanol and propanol.
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PMID:Cardiovascular effects of lysophosphatidic acid and its structural analogs in rats. 611 95

Twenty-six patients on chronic (greater than 3 months) beta-receptor blocking therapy due to ischaemic heart disease and/or hypertension were randomly distributed to a 4-day gradual withdrawal (n = 13) or a continuation of ordinary therapy until a planned cholecystectomy under neurolept anaesthesia (n = 13). Plasma-adrenaline, -noradrenaline, -potassium, -glycerol, -FFA, -insulin and b-glucose were determined perioperatively. The metabolic response to surgery was as expected with hyperglycaemia and depressed insulin levels, which did not differ significantly between the two groups of patients. Plasma-catecholamines showed the highest mean values during emergence from anaesthesia. Plasma-adrenaline and -potassium were constantly highest in the beta-receptor-blocked patients, who also showed indices of a relatively depressed lipolysis compared to patients in whom beta-receptor blockers had been withdrawn. These discrepancies between withdrawal versus continuation of preoperative beta-receptor blockade seemed to be of small clinical importance and did not oppose the present view that beta-receptor blockers should generally be continued during surgery. However, findings in individual patients suggest that beta-receptor blockade may maintain hypoglycaemia in catabolic patients.
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PMID:Long-term beta-receptor blockade--adrenergic and metabolic response to surgery and neurolept anaesthesia. 613 Jun 65

The metabolic effects of beta-adrenoceptor blocking agents during hypoglycaemia in patients prone to hypoglycaemia are of interest as diabetics are often treated with these drugs because of hypertension or angina pectoris. Compared with non-diabetics these patients also have impaired glucose compensation after hypoglycaemia, partly secondary to deficient release of glucagon. This makes the diabetics more dependent on adrenergic mechanisms to recover from low blood glucose concentrations. Non-selective beta-adrenoceptor blockade (propranolol) significantly impairs the glucose recovery rate after hypoglycaemia in insulin dependent diabetics, whereas selective beta-adrenoceptor blockade (metoprolol) does not have this side effect. The mechanism of the effect of propranolol is probably an attenuation of the gluconeogenesis secondary to deficient release of the important gluconeogenic substrates lactate and glycerol.
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PMID:Adrenergic blockade and hypoglycaemia. 613 36

The antidiuretic hormone, arginine-vasopressin (AVP), may participate in the regulation of blood pressure (BP) through its vasoconstrictor effects. In anesthetized rats, exogenous AVP induced stronger vasoconstriction in the mesenteric than in the renal vascular bed. Conversely, mesenteric but not renal vascular resistance was reduced by a vascular antagonist of AVP, d(CH2)5 VDAVP, in rats with increased endogenous AVP after anesthesia, dehydration, or injection of glycerol. Another vascular AVP-antagonist, d(CH2)5 Tyr (Me) AVP, induced a transient fall in BP in conscious primates (marmosets) after diuretic-induced volume depletion. In conscious rats with established deoxycorticosterone acetate (DOCA)/salt hypertension, d(CH2)5 Tyr (Me) AVP decreased systolic BP after acute administration. After chronic administration of this antagonist during 6 weeks after the beginning of DOCA/salt treatment, the severity of hypertension was reduced. When another, AVP-antagonist, d(CH2)5-D-Tyr (Et) VAVP, which blocks vascular and renal tubular AVP-receptors, was administered chronically, the development of DOCA/salt hypertension was prevented at the expense of severe and persistent hypernatremia. These results demonstrate that under certain conditions the vascular effects of AVP may contribute to the maintenance of BP, AVP appears to participate in the pathogenesis of DOCA/salt hypertension through both its vasoconstrictor and its antidiuretic effects.
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PMID:The significance of vasopressin as a pressor agent. 620 52

Islet-activating protein (IAP), pertussis toxin, is an oligomeric protein composed of an A-protomer and a B-oligomer. There seem to be at least two molecular mechanisms by which IAP exerts its various effects in vivo and in vitro. On the one hand, some of the effects were not significantly affected by acetamidination of the epsilon-amino groups of the lysine residues in the molecule. These include the activities in vitro (1) catalyzing ADP-ribosylation of one of the membrane proteins directly, (2) enhancing membrane adenylate cyclase activity in C6 cells, (3) reversing receptor-mediated inhibition of insulin or glycerol release from pancreatic islets or adipocytes, respectively, and the activities in vivo (4) inhibiting epinephrine-induced hyperglycemia, (5) potentiating glucose-induced hyperinsulinemia, (6) reducing hypertension and increasing the heart rate in genetically hypertensive rats. These activities are concluded to develop as a result of ADP-ribosylation catalyzed by the A-protomer which is rendered accessible to its intramembrane substrate thanks to the associated B-oligomer moiety. Thus, neither the enzymic activity of the A-protomer nor the transporting activity of the B-oligomer needs free amino groups of the lysine residues in the IAP molecule. On the other hand, additional effects of IAP, such as (1) mitogenic, (2) lymphocytosis-promoting, (3) histamine-sensitizing, (4) adjuvant and (5) vascular permeability increasing, were markedly suppressed by acetamidination of the intrapeptide lysine residues. The free epsilon-amino group of lysine would play an indispensable role in the firm (or divalent) attachment of the B-oligomer of IAP to the cell surface that is responsible for development of these activities.
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PMID:Dual mechanisms involved in development of diverse biological activities of islet-activating protein, pertussis toxin, as revealed by chemical modification of lysine residues in the toxin molecule. 638 83


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