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

Plasma values of atrial natriuretic factor (ANF) were evaluated in 31 women with pregnancy-induced hypertension (PIH) and 31 normal pregnant women at the same age of gestation. In 27 women with PIH and 27 normal pregnant women forearm venous tone (FVT) was evaluated by Strain Gauge Plethysmography. Forearm vascular resistance (FVR) was measured as the ratio of mean blood pressure (MBP) to forearm blood flow. In addition Cardiac Index (CI) by means of transthoracic electrical bioimpedance and total peripheral vascular resistance (TPR) (with the Frank Equation) were also measured. In comparison with the normal pregnant women, the women with PIH had similar values of hematocrit (as an index of plasma volume) and significantly higher levels of FVR and TPR, while ANF plasma values did not differ significantly. Subdividing the women with PIH in relation to the presence of proteinuria (greater than or equal to 0.3 g/l), those with proteinuria, in addition to significantly higher levels of FVR and TPR, had significantly higher levels of FVT than normal pregnant women, while ANF plasma values were higher even though the difference was only near the level of significance. Hypertensive women with proteinuria also had higher values of FVT than hypertensive women without proteinuria. By means of multiple regression ANF did not show any significant correlations with hematocrit or sodium excretion. Hypertension with proteinuria seems to represent a more severe form of the disease in which, in addition to the probable influence of other factors such as the renin-angiotensin and prostaglandin systems, a greater increase in peripheral sympathetic tone than in hypertension alone appears to be present, causing a reduction in venous compliance in addition to the elevation in FVR and TPR, with increase in central blood volume and atrial stretch. This may explain the higher ANF plasma levels in these patients in comparison with normal pregnant women, even though the absence of a significant correlation of ANF with hematocrit and the fact that ANF increase was only near the level of significance may suggest a change in the relation between ANF secretion and atrial volume receptors in pregnancy either normal or complicated by hypertension. ANF does not seem to play an important role in water and sodium excretion in PIH probably because of the presence of very high plasma levels of hormones such as aldosterone, progesterone and oestriol which, together with renal prostaglandins, seem to be involved in diuresis and natriuresis in pregnancy.
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PMID:Plasma concentrations of atrial natriuretic factor and hemodynamics in pregnancy-induced hypertension. 183 84

Cadmium (Cd) exposure is known to alter cardiovascular function and has been implicated in the etiology of hypertension. Atrial natriuretic peptide (ANP), a hormone secreted by the heart, has been established as a diuretic, natriuretic, smooth muscle relaxant and may be a modulator of central cardiovascular regulation. The effects of Cd treatment on ANP levels in select tissues were studied as a possible mechanism underlying Cd-induced cardiovascular toxicity. Male rats were injected with CdCl2 (0.01, 0.1, 0.5 or 1.0 mg/kg, i.p.), twice a day for 7 days and then maintained for a period of 30 days. On experimental day 38 plasma renin activity and plasma ANP content were not significantly altered. The high dose of Cd significantly decreased plasma aldosterone levels and atrial ANP levels on day 38. Hypothalamic ANP was significantly decreased at the 0.1, 0.5 and 1.0 mg/kg doses. Throughout the 37-day period, water consumption was not altered. Urine output was decreased in all treatment groups on day 37. The results indicate that Cd can alter select tissue content of the ANP and this interaction may play an important role in the cardiovascular effects of CD.
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PMID:Alteration of atrial natriuretic peptide levels by short term cadmium treatment. 183 92

Hypertension is linked to the development of nephropathy in Type 1 diabetes. Total exchangeable sodium is elevated in patients with Type 1 diabetes in good metabolic control, and correlates with blood pressure. Atrial natriuretic factor has been shown to have effects on sodium and blood pressure homeostasis in man. Basal and NaCl-stimulated plasma atrial natriuretic factor was therefore studied in 33 patients with Type 1 diabetes. Seventeen had no evidence of nephropathy, 11 had incipient nephropathy (albumin excretion rate 20-199 micrograms min-1) and five had overt nephropathy. Seventeen age- and sex-matched normal control subjects were also studied. Subjects fasted from 2200 h, rose at 0745 h and remained ambulant until 0945 h. After 15 min supine, 2 l 0.15 mmol l-1 NaCl was infused over 4 h. Basal erect (0945 h) plasma atrial natriuretic factor was 4.2 +/- 0.5, 3.5 +/- 0.4, 2.5 +/- 0.2, and 2.5 +/- 0.3 pmol l-1 in the control, non-nephropathic, incipient-nephropathic, and overt nephropathic diabetic groups, respectively (all NS). Levels in all groups increased in response to NaCl infusion, and the responses were not different between groups. Urinary sodium excretion for 12 h before NaCl infusion was not different between groups, but during the 12 h after the start of the infusion was significantly (p less than 0.05) less in the Type 1 diabetic group without nephropathy than in the control group. These results suggest that atrial natriuretic factor does not play a major role in the development of changes in sodium balance which are associated with Type 1 diabetes and nephropathy.
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PMID:Basal and stimulated plasma atrial natriuretic factor in patients with type 1 diabetes with and without nephropathy. 183 69

In order to evaluate the effects of atrial natriuretic factor (ANF) infusion on plasma insulin (IRI) in hypertension, 32 essential hypertensives (aged 40 to 62 years) were studied. After 1 week of pharmacologic washout under normal sodium intake (120 mEq of Na+/day), patients were randomly assigned to receive either ANF (0.04 micrograms/kg/min) or its vehicle (50 mL of isotonic saline) over a 60-min period in supine position. Plasma IRI and glucose were measured at -60, 0, 20, 40, 60, 120, 180, and 240 min (infusion time: from 0 to 60 min). Plasma levels of IRI and glucose did not change significantly during ANF infusion. On the contrary, after ANF discontinuation plasma IRI rose from levels of 13.5 +/- 6.4 microU/mL at 60 min to values of 20.1 +/- 11.3 microU/mL at 240 min (P less than .0001 v time 0). Plasma glucose showed a similar behavior, increasing from values of 100.4 +/- 5.0 mg/dL at 60 min to values of 120.0 +/- 5.1 mg/dL at 240 min (P less than .02 v time 0). Our findings suggest that ANF did not influence insulin release in hypertensives. The increase of plasma glucose and IRI observed after ANF discontinuation could be due to the relapse of sympathetic activity, suppressed during ANF infusion.
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PMID:Plasma insulin levels do not change during atrial natriuretic factor infusion in human essential hypertensives. 183 90

Subjects with Type 2 diabetes have been reported to have elevated total exchangeable sodium when compared with normal subjects. Sodium retention may contribute to the development of hypertension in these subjects. Atrial natriuretic factor may play a role in sodium and blood pressure homeostasis in Type 2 diabetes. We have studied plasma atrial natriuretic factor in 17 subjects with Type 2 diabetes (9M:8F; aged 49 +/- 2 years) (mean +/- SE) and in 17 age- (49 +/- 2 years) and sex-matched controls. Mean fasting blood sugar was 8.3 +/- 0.6 mmol l-1 in the diabetic subjects. After fasting from 2200h, subjects remained upright from 0745h until 0945h when blood was taken for plasma atrial natriuretic factor, plasma renin activity and serum aldosterone. Two litres of 0.15 mmol l-1 NaCl was infused intravenously between 1000h and 1400h while the subjects remained supine. Blood was taken hourly. At 0945h plasma atrial natriuretic factor was 3.8 +/- 0.4 pmol l-1 in diabetic subjects and 6.1 +/- 1.6 pmol l-1 in controls (NS), at 1000h after 15 mins supine 3.5 +/- 0.3 and 7.9 +/- 2.3 pmol l-1 respectively (p < 0.05) and increased to 9.4 +/- 1.5 and 9.4 +/- 1.2 pmol l-1 in diabetic subjects and controls at 1400h (NS; both p < 0.01 vs basal values). Serum aldosterone, plasma renin activity, blood pressure and urinary sodium output for 12h before, 4h during and 8h after the NaCl infusion were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Basal and stimulated plasma atrial natriuretic factor in type 2 diabetes. 184 25

Cardiac atria and, under certain circumstances, also ventricles produce and secrete into the circulation atrial natriuretic factor (ANF). ANF exerts a significantly natriuretic, myorelaxant, renin-, aldosterone-, and vasopressin-inhibiting effect and acts as a neurotransmitter in the central and autonomous nervous systems. Expansion of the extracellular volume stimulates secretion of ANF which consequently contributes to renal excretion of sodium and water. The renal effect of ANF is apparently modulated by interaction with other mechanisms. ANF concentration in peripheral blood is the product of its secretion by the heart and degradation by peripheral tissues. In ascitic liver cirrhosis, the decreased splanchnic bed uptake may contribute to the increase in plasma ANF concentration observed. Insufficient production or secretion of ANF are not likely to be the primary etiopathogenic mechanism of arterial hypertension. In the course of development of hypertension, ANF is mobilized as a corrective-adaptive mechanism in an effort to normalize the raised BP, extracellular volume or circulating pressor agents. Through its production of ANF, the heart possess an important endocrine function markedly affecting pressure, electrolyte and volume homeostasis.
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PMID:Role of the heart as an endocrine organ. 184 37

Atrial natriuretic peptide (ANP) exhibits a wide spectrum of cardiovascular, endocrine, metabolic and renal actions. cGMP is the major mediator of ANP at the cellular level and only tissues possessing particulate guanylate cyclase appear to present ANP-induced actions. Three types of ANP receptors have recently been cloned. Two of them (A and B receptors) are homologous and contain guanylate cyclase catalytic domains. The C receptor could possibly regulate the metabolic fate of ANP. Data obtained by the radiation inactivation method suggest the presence of an inter- or intramolecular inhibitory component of nearly 90 kilodaltons that represses the catalytic activity of guanylate cyclase within its membrane environment. The mechanism of guanylate cyclase stimulation by ANP could involve this inhibitory component. Preliminary data suggest that the hyperresponsiveness of the particulate guanylate cyclase/cGMP system in hypertension occurs through modulation of the inhibitory component.
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PMID:Cell biology of atrial natriuretic peptide. 184 28

Whole body clearance of atrial natriuretic factor is due to both receptor uptake and enzymatic degradation initiated by neutral endopeptidase 24.11. The effects of neutral endopeptidase inhibition have been studied in seven sodium-replete sheep using SCH 39370, a specific and potent inhibitor of neutral endopeptidase, in the presence or absence of exogenous hormone [rat ANF-(101-126), 2.4 pmol/kg/min for 2 hours]. SCH 39370 alone (2.5 mg/kg bolus) increased plasma atrial natriuretic factor and plasma cyclic GMP levels, lowered arterial pressure for periods beyond changes in plasma atrial natriuretic factor or cyclic GMP, and suppressed both plasma aldosterone and cortisol levels when compared with vehicle injections. The effects of SCH 39370 were similar to or exceeded those of atrial natriuretic factor infusions, which induced significantly greater increases in plasma atrial natriuretic factor (p = 0.01). Neither agent alone was natriuretic. When SCH 39370 and atrial natriuretic factor were given together, plasma cyclic GMP but not atrial natriuretic factor levels were increased (p = 0.013) compared with atrial natriuretic factor infusion alone, and the half-life was prolonged (p = 0.002) in the presence of SCH 39370. The hypotensive response was greater than that induced by atrial natriuretic factor alone (p = 0.03) but not different from SCH 39370 alone. Inhibitory effects of SCH 39370 on aldosterone levels were similar in the presence of absence of exogenous atrial natriuretic factor.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 May
PMID:Hemodynamic and hormonal effects of neutral endopeptidase inhibitor SCH 39370 in sheep. 185 Jul 15

Angiotensin-converting enzyme (ACE) and enkephalinase, two cell surface metallopeptidases, are responsible for angiotensin II formation and atrial natriuretic factor (ANF) degradation, respectively, and thereby play a critical role in the metabolism of hormonal peptides exerting essentially opposite actions in cardiovascular regulations. To affect simultaneously both hormonal systems by a single molecular structure, we have designed glycoprilat and alatrioprilat [(S)-N-[3-(3,4-methylene-dioxyphenyl)-2-(mercaptomethyl)-1-oxoprop yl] glycine and -alanine, respectively]. In vitro the two compounds inhibit both ACE and enkephalinase activities with similar, nanomolar potencies, and in vivo, glycopril and alatriopril, the corresponding diester prodrugs, occupy the two enzyme molecules in lung at similar low dosages (0.2-0.5 mg/kg of body weight, per os). The high potency of these compounds is attributable to interaction of the methylenedioxy group with the S1 subsite of ACE and of the aromatic ring with the S1' subsite of enkephalinase. In rodents, low doses of these mixed inhibitors exert typical actions of ACE inhibitors--i.e., prevention of angiotensin I-induced hypertension--as well as of enkephalinase inhibitors--i.e., protection from 125I-ANF degradation or enhancement of diuresis and natriuresis following acute extracellular volume expansion. In view of the known counterbalanced physiological actions of the two hormonal peptides, whose metabolism is controlled by ACE and enkephalinase, mixed inhibitors of the two peptidases show promise for the treatment of various cardiovascular and salt-retention disorders.
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PMID:Mixed inhibitors of angiotensin-converting enzyme (EC 3.4.15.1) and enkephalinase (EC 3.4.24.11): rational design, properties, and potential cardiovascular applications of glycopril and alatriopril. 185 98

In an attempt to explore pathophysiological mechanisms relevant for the development for future primary hypertension, we investigated young normotensive men with positive family histories of hypertension (PFH) regarding blood pressure, body weight, systemic and renal haemodynamics as well as cardiovascular hormones and sodium homeostasis. Sixteen subjects with PFH and thirteen controls with negative family histories (NFH), matched for age and body weight were investigated at age 31 and after five years. Blood pressure and heart rate did not differ between the two groups at the first or follow-up examination. At follow-up body weight had increased and a positive correlation between blood pressure and body mass index was found in subjects with PFH, while subjects with NFH had unchanged blood pressure and body weight. Initially, intraerythrocyte sodium content was increased in subjects with PFH, however, at follow-up intraerythrocyte sodium content did not differ between the two groups. At follow-up systemic and renal haemodynamics and sodium homeostasis were investigated in fifteen subjects with PFH and in twenty-nine controls matched for age (36 +/- 5 year) and with NFH. The control group was divided into one group matched for body mass index (n = 15) and one group with normal body mass index (n = 14). Blood pressure and central venous pressure were measured during bolus injections of phenylephrine and during an acute saline/fluid load (1000ml 0.9% NaCl within 10 min). Renal haemodynamics and blood pressure were measured during low doses (0.1 and 0.5 ng/min/kg) continuous infusions of angiotensin II (AII). At baseline blood pressure, body weight and sodium excretion were higher in subjects with PFH and matched controls as compared with lean controls. Calf and forearm haemodynamics (pletysmography), plasma catecholamines, plasma renin activity, angiotensin II, aldosterone, blood volume and erythrocyte sodium efflux rate constant did not differ between the three groups. Circulating atrial natriuretic peptide was higher in subjects with PFH than in the two control groups. In subjects with PFH there was a negative correlation between renal sodium excretion at baseline and the ouabain-sensitive sodium efflux rate constant. During the acute saline/fluid load central venous pressure and systolic blood pressure increased more and venous vascular compliance (ml/mmHg/kg) was reduced in PFH. Atrial natriuretic peptide release and renal sodium excretion were blunted during saline/fluid load in subjects with PFH as compared with the two control groups. Renal blood flow and renal vascular resistance did not differ at baseline. Glomerular filtration rate was somewhat higher in PFH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Family history and pathophysiological mechanisms of primary hypertension. Studies in non-hypertensive young men with positive and negative family histories of hypertension. 188 13


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