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

Vasoactive hormones acting as endocrine, neuroendocrine, or local hormonal systems (intracrine, autocrine, and paracrine) are an important component of the many factors that regulate blood pressure. Hypertension may be the result of an alteration in the balance between vasodepressor and vasopressor hormonal systems. Changes in this balance could be due to genetic factors such as mutations in one of the genes of the vasoactive system or environmental factors that alter the synthesis and release of one or more vasoactive hormones. Endocrine and neuroendocrine vasopressor hormonal systems, such as the renin-angiotensin system and catecholamines, play a well-established and important role in the regulation of blood pressure and the pathogenesis of some secondary forms of hypertension. The blockade of such systems has already resulted in effective antihypertensive treatment. The role of local hormonal systems is less well established; however, recent evidence suggests they also play an important role in the regulation of blood pressure and the pathogenesis of hypertension. Some vasopressor hormonal systems, such as the renin-angiotensin system, can act as both endocrine or local hormonal systems. Work using transgenic rats harboring the mouse Ren-2 gene has conclusively demonstrated that the renin-angiotensin system, acting as a local hormonal system, has the capability to cause severe hypertension. Whether this model of experimental hypertension mimics any type of human hypertension is not known. Vasodepressor hormones such as kinins, prostaglandins, and endothelium-derived relaxing factor (EDRF) act mainly as local hormonal systems, with the notable exception of atrial natriuretic factor, which may act as both an endocrine and a local hormone. The tissue kallikrein-kinin system, acting either directly or via paracrine eicosanoids or EDRF, participates in local regulation of the circulation, renal function, and the acute antihypertensive effect of angiotensin converting enzyme inhibitors. A restriction fragment length polymorphism (RFLP) that distinguishes the kallikrein gene family of a strain of spontaneously hypertensive rats (SHR) from normotensive Brown Norway rats has been identified. In a set of 32 recombinant inbred strains derived from these SHR and Brown Norway strains, the RFLP marking the kallikrein gene family of SHR cosegregated with an increase in blood pressure. Also, in a study of Utah families it was found that a dominant-allele kallikrein gene expressed as high urinary kallikrein excretion was associated with a decreased risk of essential hypertension. In conclusion, vasopressor and vasodepressor hormones, acting not only as endocrine but also as local hormones, play an important role in the regulation of blood pressure and the pathogenesis of hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
Hypertension 1991 Sep
PMID:Local hormonal factors (intracrine, autocrine, and paracrine) in hypertension. 188 59

We compared the tubular transport of sodium and the erythrocyte sodium-lithium countertransport activity in hypertensive patients with autosomal dominant polycystic kidney disease (ADPKD) and in normotensive control subjects. In addition, we assessed the effects of inhibition of converting enzyme on renal hemodynamics and sodium excretion in hypertensive patients with ADPKD to provide information on mechanisms responsible for the increased renal vascular resistance and filtration fraction and the adjustment of the pressure-natriuresis relationship during saline expansion, observed in patients with ADPKD, hypertension, and preserved renal function. In comparison with normotensive control subjects, the hypertensive patients with ADPKD had lower renal plasma flows, higher renal vascular resistances and filtration fractions, and similar proximal and distal fractional reabsorptions of sodium. The administration of enalapril resulted in significant increases in the renal plasma flow and significant reductions in mean arterial pressure, renal vascular resistance, and filtration fraction, but the glomerular filtration rate remained unchanged. Despite the significant reduction in mean arterial pressure during inhibition of converting enzyme, the distal fractional reabsorption of sodium decreased while the total fractional excretion of sodium remained unchanged or increased slightly. No significant differences were detected between the normotensive control subjects and the hypertensive patients with ADPKD in erythrocyte sodium-lithium countertransport activity, plasma renin activity, plasma aldosterone concentration, or atrial natriuretic factor. These results suggest that the renal renin-angiotensin system plays a central role in the alterations in renal hemodynamics and sodium management associated with the development of hypertension in ADPKD.
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PMID:Effect of inhibition of converting enzyme on renal hemodynamics and sodium management in polycystic kidney disease. 192 83

To investigate the possible relationship of hypertension and the N-terminus of the atrial natriuretic factor (ANF) prohormone which contains two peptides [i.e. pro ANF-(1-30) and pro-ANF-(31-67)] with blood pressure-lowering effects, we examined the circulating levels of the N-terminus of the ANF prohormone in three patients with pheochromocytomas before surgery, during an increase in their blood pressure with surgical manipulation of their tumors, and after surgery when their blood pressures returned to normal. The circulating levels of the whole N-terminus [amino acids 1-98; pro-ANF-(1-98)] and pro-ANF-(31-67) from the midportion of the N-terminus of the ANF prohormone were increased 2-fold in patients with both extraadrenal and intraadrenal pheochromocytomas. In both the intraadrenal and extraadrenal patients N-terminus [pro-ANF-(1-98)] and pro-ANF-(31-67) circulating levels increased further during surgical manipulation and returned to normal after surgical removal of their respective tumors. Each of these pheochromocytomas was found to have pro-ANF-(1-30) and -(31-67)-binding sites that were functional, since they could enhance the guanylate cyclase-cGMP system 2-fold in these pheochromocytomas. The entire 126 amino acids of the prohormone were present within each of the pheochromocytomas, since both the whole N-terminus and C-terminus (i.e. ANF) of the prohormone were present. Examination of the pheochromocytomas by electron microscopy revealed electron-dense granules similar to those in the heart, which have been associated with the synthesis and storage of the ANF prohormone. We conclude that 1) the whole N-terminus [pro-ANF-(1-98)] and pro-ANF-(31-67) of the ANF prohormone circulate at higher concentrations in persons with pheochromocytomas and return to normal with removal of the tumors; 2) pheochromocytomas contain specific binding sites for pro-ANF-(1-30) and -(31-67); 3) these binding sites are functional, since pro-ANF-(1-30) and -(31-67) could enhance the enzyme guanylate cyclase within these tumors; and 4) the entire 126 amino acids of the ANF prohormone are present within these tumors, which have electron-dense granules associated with polypeptide hormone synthesis, suggesting that the ANF prohormone is being synthesized within the pheochromocytomas.
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PMID:Increased circulating concentration of the N-terminus of the atrial natriuretic factor prohormone in persons with pheochromocytomas. 197 56

Although dietary salt restriction is often valuable as sole or adjunctive therapy of hypertensive disorders, it is abundantly clear that hypertensive patients comprise a heterogeneous group with regard to salt sensitivity of blood pressure. This is apparent despite the many methodological obstacles to defining salt sensitivity in an individual patient. Currently, dietary trial is the only sure means of defining a given patient as responsive to salt restriction. Easily definable markers of salt sensitivity would allow appropriate targeting of this rather ponderous therapy. Promising leads include the assessment of membrane ion transporters such as sodium-lithium exchange and of the activity of the renin-angiotensin system, including the phenomenon of "non-modulating" hypertension and other volume regulatory hormones such as atrial natriuretic factor. Although less intensively studied than in hypertensive patients, the blood pressure response of normal subjects to salt restriction is also marked by great variability. Given the possibility of deleterious consequences of population-wide salt restriction for at least some people in a setting such as the United States, it seems imprudent to recommend such a policy before its proven worth has been demonstrated by clinical trial. Pending such evidence and the development of markers, salt restriction should be reserved for those in whom it is of demonstrated efficacy.
Hypertension 1991 Jan
PMID:Dietary salt and blood pressure. A perspective. 198 20

The decrease in renal blood flow (RBF) observed in patients with hypertension can be increased with converting enzyme inhibition (CEI). It is unknown whether the decrease in RBF observed with age can also be increased with CEI. This study compared the short- and long-term effects of captopril monotherapy in young (less than 50 years) and old (greater than 65 years) hypertensive patients. Captopril effectively decreased blood pressure in both groups (diastolic blood pressure less than 90 mm Hg), with the young patients requiring a lower dose (.7 mg/kg) than the elderly patients (1.2 mg/kg). Creatinine and para-aminohippurate clearances were maintained in both groups, with a decrease in renal vascular resistance being observed in the younger patients. Serum aldosterone levels fell significantly after each dose of captopril at all phases of the study, with no change observed in plasma renin levels. Atrial natriuretic peptide (ANP) level was increased in the elderly patients receiving placebo (48.8 +/- 8 pg/mL) when compared with the young subjects (24 +/- 3.8 pg/mL). Captopril did not alter ANP levels in either group.
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PMID:Long-term captopril in young and old patients with mild hypertension. 204 30

Atrial natriuretic factor (ANF) is a hormone with the physiological characteristics of a regulator of body fluid volume. It is potent, has a short duration of action, and responds to a physiologically relevant stimulus in a negative feedback-controlled system. It can act directly or indirectly (via inhibition of aldosterone biosynthesis) on the kidney to alter sodium transport and may regulate fluid distribution within the extracellular space. The peptide circulates at low (nanomolar) levels, and recent studies with renal inner medullary cells document relevant receptor binding and second messenger activation in this concentration range. In vivo data support a direct action on the kidney to enhance natriuresis, and blockade of a primary catabolic pathway for ANF within the kidney results in augmented natriuresis at concurrent endogenous peptide concentrations. Long-term, low dose infusion directly into the renal artery of conscious dogs supports a physiological action of ANF to promote urinary sodium excretion. Nevertheless, under certain circumstances, natriuresis does not occur even at high circulating levels of ANF. Apparently other factors such as renal perfusion pressure, volume status, and renal nerve activity are important in determining the natriuretic response to a given level of peptide. We hypothesize that the role played by ANF in volume regulation is highly complex, and the kidney responds with increased sodium excretion only when a constellation of variables is appropriately arrayed. That is, ANF is a necessary, but not sufficient, condition to induce natriuresis.
Hypertension 1990 Jan
PMID:Atrial natriuretic factor plays a significant role in body fluid homeostasis. 213 43

Although much experimental evidence is consistent with the concept that atrial natriuretic factor (atriopeptin) is an important physiological regulator of renal sodium excretion, this hypothesis remains unproven. Indeed, a rapidly expanding collection of experimental data appears to be more compatible with the opposite conclusion, namely that circulating atriopeptin exerts only a trivial effect on renal sodium excretion during normal day-to-day living conditions. In this review, the substantial evidence demonstrating that elevations of plasma atriopeptin from threefold to 13-fold produce only a slowly developing and relatively modest natriuresis is reassessed in light of recently published data indicating that the acute intake of food (the pathway by which essentially all sodium enters the body under normal living conditions) does not increase circulating atriopeptin. These considerations imply that atriopeptin does not contribute to the process that elicits a postprandial natriuresis, a process that presumably is of primary importance in the physiological regulation of sodium balance. In addition, consideration is given to a number of common physiological, experimental, and pathophysiological conditions in which circulating atriopeptin does not correlate with renal sodium excretion. This lack of correlation implies that atriopeptin is not an important regulator of sodium excretion in these situations.
Hypertension 1990 Jan
PMID:Evidence that atriopeptin is not a physiological regulator of sodium excretion. 213 44

The atrial natriuretic factor (ANF) is a hormone whose effects and mode of secretion have been determined. But its exact role in the regulation of volemia in comparison with that of the renin-angiotensin system is still to be defined. Studies of human diseases associated with an increase of ANF plasma concentration may help reach this goal. The mechanisms resulting in elevated ANF plasma concentrations (increase of secretion, decrease of catabolism of the hormone) and the effects of these high levels of ANF on renal functions and circulation are analysed in chronic cardiac failure, mitral stenosis, pulmonary artery hypertension, acute tachycardias, chronic and acute renal failures and in the course of cardiac transplantation. The therapeutic usefulness of drugs inhibiting ANF catabolism (blockers of the clearance receptors for ANF and inhibitors of the enzymes degrading ANF) is also considered.
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PMID:[Atrial natriuretic factor. Role in the physiopathology of cardiac and renal diseases]. 213 35

In feral populations of African green monkeys or vervets (Cercopithecus aethiops), between 5 and 15% of adults have spontaneously elevated blood pressure (BP). We report here the initial biological and pharmacological characterization of this potential animal model of hypertension. Captive male monkeys with elevated systolic pressures show a modest pressure increase in response to stressors such as capture, phlebotomy and cold challenge. Acute captopril administration lowers BP in monkeys with high blood pressure (HBP), but has no effect on BP in control animals. Furosemide does not acutely reduce BP. Animals with elevated BPs have lower levels of angiotensin II than do age- and weight-matched controls. An acute infusion of atrial natriuretic factor (ANF) diminishes BP and stimulates urinary output in control and HBP vervets. However, both effects are more pronounced in animals with HBP. Heart rate is not affected by any of the experimental manipulations. Taken together, these data suggest that African green monkeys with spontaneously elevated BP may be a useful experimental model for particular types of human hypertension. Additional studies are required to complete the endocrine and pharmacological characterization of individual animals with HBP.
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PMID:Characterization of a primate model of hypertension. The response of hypertensive and normotensive male vervets (Cercopithecus aethiops) to cold pressor stress, captopril administration, and acute bolus of atrial natriuretic factor. 213 42

The modulation exerted by atrial natriuretic factor (ANF) on the cardiac and vascular influences of arterial baroreceptors was investigated in two groups of unanesthetized, chronically instrumented normotensive rats. In group 1, the reflex control of heart rate was assessed by graded baroreceptor stimulations and deactivations obtained by intravenous boluses of phenylephrine and nitroprusside. Under either circumstance, baroreceptor reflex sensitivity was expressed as the linear regression slope relating the chronotropic responses to the drug-induced mean arterial pressure changes. In group 2, right common carotid occlusion was performed in rats with their aortic and left carotid sinus baroreceptors denervated to assess the baroreceptor control of blood pressure; the reflex response was quantitated as the peak blood pressure rise observed during the maneuver. The reflex studies were performed before and during atriopeptin III infusion (0.15-0.20 micrograms/kg/min for 60 minutes). ANF augmented the bradycardic response to phenylephrine by 102.5 +/- 29% (p less than 0.01), reduced the tachycardic response to nitroprusside by 67.7 +/- 6.4% (p less than 0.01), and failed to modify the pressor response to carotid occlusion (-6.8 +/- 2.1%, p = NS). In a separate group of rats infused with low dose nitroprusside, no change in the baroreceptor-heart rate reflex was observed. ANF infusion (0.20 micrograms/kg/min) performed in further separate groups of conscious rats raised plasma ANF to 480 +/- 58 fmol/ml. Values in control vehicle-infused rats were 50 +/- 8 fmol/ml. Vascular reactivity (pressor response to intravenous phenylephrine boluses in anesthetized, sinoaortic-denervated rats) was only minimally reduced by ANF.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Feb
PMID:Atrial natriuretic factor and arterial baroreceptor reflexes in unanesthetized rats. 213 28


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