Urinary excretion of atrial natriuretic peptide during saline infusion and supraventricular tachycardia.
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Atrial Natriuretic Factor↗
Biomedical subjects
H Yoshimi
Publications and source records attributed to H Yoshimi.
[Role of the renin-angiotensin aldosterone system in the development of hypertension].
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Humans↗
Binding and receptor down-regulation of a novel vasoconstrictor endothelin in cultured rat vascular smooth muscle cells.
Binding of a novel endothelium-derived vasoconstrictor endothelin (ET) and the regulation of its receptor were studied in cultured rat vascular smooth muscle cells. 125I-labeled-ET bound to the cells was resistant to acid extraction and the majority of the acid-resistant compartment was extractable with chloroform/methanol with minimal degradation. Autoradiographic studies using electron microscopy revealed that the grains were predominantly localized in the plasma membranes, but some were adjacent to and within the lysosome. Pretreatment with ET resulted in a substantial reduction of ET receptor number without changing its binding affinity. ET-induced increase in cytosolic free Ca2+ levels [( Ca2+]i] was absent or attenuated in the ET-pretreated cells. These data suggest that tight association of ET with its receptor is due to a strong interaction of its hydrophobic domain with the membrane lipids and/or its internalization within cells and that down-regulation of ET receptor is functionally linked to decreased ET-induced [Ca2+]i response.
Animals↗
Endothelin is a potent secretagogue for atrial natriuretic peptide in cultured rat atrial myocytes.
Using cultured neonatal rat atrial cardiocytes, we have studied the effect of synthetic porcine endothelin (pET), a novel potent vasoconstrictor isolated from endothelial cells, on the release of immunoreactive (IR) rat atrial natriuretic peptide (rANP). pET stimulated IR-rANP secretion in a dose-dependent manner (10(-10)-10(-7) M) with an approximate half-maximally stimulatory dose of 2 x 10(-10) M. The pET-induced IR-rANP secretion was attenuated by Ca2+-channel blocker nicardipine, but no further stimulation was induced when combined with a Ca2+-channel agonist BAY-K 8644. pET in combination with tetradecanoyl-phorbol-acetate resulted in a synergistic effect on IR-rANP secretion. These data suggest that ET may play as an endogenous secretagogue for rANP by modulating Ca2+ influx through the voltage-dependent Ca2+-channels in atrial cardiocytes.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Cellular mechanism of action by a novel vasoconstrictor endothelin in cultured rat vascular smooth muscle cells.
Specific binding sites for synthetic porcine endothelin (pET), a novel potent vasoconstrictor peptide isolated from the supernatant of cultured porcine endothelial cells, and its effects on cytosolic free Ca2+ concentrations ([Ca2+]i) and phosphatidylinositol (PI) response were studied in cultured rat aortic vascular smooth muscle cells (VSMC). Binding of 125I-labeled-pET to rat VSMC was time- and temperature-dependent and the cell-bound 125I-labeled-pET was resistant to dissociate. Scatchard analysis of binding studies indicated the presence of a single class of high-affinity binding sites: the apparent Kd was 2-4 X 10(-10) M and the maximal binding capacity was 11,000-13,000 sites/cell. The binding was highly specific for pET because neither well-recognized vasoconstrictors, peptide neurotoxins, nor Ca2+-channel blockers affected the binding. pET dose-dependently (10(-9)-10(-7) M) induced a transient and sustained increase in [Ca2+]i in fura-2-loaded cells of which effect was largely dependent on extracellular Ca2+, whereas it had no significant effect on PI response in 3H-myoinositol-prelabeled cells. The present data clearly demonstrates the presence of specific receptors for pET distinct from those of the well-recognized vasoconstrictors and voltage-dependent Ca2+-channels in cultured rat VSMC, and suggest that pET-induced increase in [Ca2+]i is involved in the mechanism of its vasoconstriction.
Animals↗
Phorbol ester modulates serotonin receptor-mediated increases in inositol phosphate production and calcium mobilization in cultured rat vascular smooth muscle cells.
The effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on serotonin-induced inositol phosphate (IP) accumulation and intracellular free Ca2+ concentrations [( Ca2+]i) was investigated in cultured rat vascular smooth muscle cells. Pretreatment with TPA had no effect on basal levels of both IP production and [Ca2+]i, whereas it significantly attenuated serotonin-induced increases in both IP production and [Ca2+]i. These data suggest that protein kinase C is involved in the negative feedback control of serotonin-induced rises in both IP production and [Ca2+]i.
Animals↗
A novel human plasma factor(s) capable of mobilizing intracellular Ca2+ in cultured rat vascular smooth muscle cells.
Using fura-2-loaded rat vascular smooth muscle cells (VSMCs) in culture, we have attempted to partially purify and characterize yet unidentified factor(s) from normal human plasma that stimulates cytoplasmic free Ca2+ concentration ([Ca2+]i). The plasma extract caused an immediate and transient increase of [Ca2+]i in a dose-dependent manner, of which effect was not prevented by pretreatment with either any of receptor antagonists for -adrenergic agonist, angiotensin II, arginine vasopressin, serotonin, thromboxane A2, or with EGTA and nifedipine. This novel plasma factor(s) was heat-stable and completely inactivated by pronase E, suggesting its protein nature. Furthermore, plasma extracts dose-dependently stimulated the accumulation of [3H] inositol phosphates in rat VSMCs. Sephadex G-50 gel chromatography of plasma extracts resolved one major component (mol wt 13,000) and two minor components with larger (greater than 30,000) and smaller (3,000) mol wt. Present study demonstrates the presence of hitherto unidentified plasma factor(s) with size heterogeneity capable of stimulating both mobilization of [Ca2+]i and breakdown of phosphatidylinositol-4,5-biphosphates in rat VSMCs.
Animals↗
Calcitonin gene-related peptide receptor in cultured vascular smooth muscle and endothelial cells.
Using 125I-labeled-Tyr0-rat(r)-calcitonin gene-related peptide (CGRP), a potent vasodilatory neuropeptide, we have identified and characterized specific binding sites for CGRP in cultured rat vascular smooth muscle cells (VSMC) and bovine endothelial cells (EC). rCGRP and human (h) CGRP equipotently inhibited 125I-rCGRP binding to both cells, but human calcitonin (hCT) was less potent and other unrelated polypeptides were ineffective. Both rCGRP and hCGRP, but not hCT, equally stimulated intracellular cAMP generation in both cells distinct from beta-adrenergic receptor-mediated mechanism, although they had no effect on cGMP generation in either cell or synthesis of prostacyclin in EC. Autoradiograph of affinity-labeled cell membranes revealed that 125I-rCGRP interacts with a single binding component of almost identical molecular size (approximately 60-kDa) in both cells under reducing and nonreducing conditions. The present study demonstrates for the first time the presence of CGRP receptors in cultured VSMC and EC, functionally coupled to adenylate cyclase system distinct from beta-adrenergic receptors. It is suggested that CGRP-induced vasorelaxation may be mediated partly by cAMP-dependent and/or endothelium-dependent mechanism.
Animals↗
Effects of protein kinase inhibitors on growth factor-stimulated DNA synthesis in cultured rat vascular smooth muscle cells.
The effects of H-7 and ML-9, inhibitors of protein kinase C and myosin light-chain kinase, respectively, on DNA synthesis stimulated by platelet-derived growth factor (PDGF) and epidermal growth factor (EGF) were studied in cultured rat vascular smooth muscle cells (VSMC). H-7 and ML-9 significantly inhibited PDGF-stimulated DNA synthesis in lower concentrations, while both compounds were only effective in inhibiting EGF-induced DNA synthesis in higher concentrations. These data suggest that protein kinase C and myosin light-chain kinase activated by PDGF play a more important role in cell proliferation of VSMC than EGF.
Animals↗
Measurement of left atrial systolic time intervals in hypertensive patients using Doppler echocardiography: relation to fourth heart sound and left ventricular wall thickness.
The concept of left atrial systolic time intervals and Doppler echocardiography were used in a quantitative assessment of left atrial function in relation to the presence or absence of a fourth heart sound and to left ventricular hypertrophy in 47 patients with hypertension. Left atrial systolic time interval indexes included atrial pre-ejection period (the time between the onset of an electrocardiographic P wave and the onset of left ventricular inflow during atrial systole [A wave]), corrected atrial pre-ejection period (the atrial pre-ejection period divided by the duration of the P wave), and atrial ejection time (the time between the onset and cessation of the A wave). Twenty-one patients with a fourth heart sound on the phonocardiogram had a shorter atrial pre-ejection period (81 +/- 10 versus 89 +/- 14 ms p less than 0.05) and a corrected atrial pre-ejection period (66 +/- 17 versus 83 +/- 18 ms, p less than 0.01), as well as a longer atrial ejection time (147 +/- 15 versus 126 +/- 13 ms, p less than 0.001) than did 26 patients without a fourth heart sound. The ratio of atrial pre-ejection period to atrial ejection time and that of corrected atrial pre-ejection period to atrial ejection time was smaller in patients with than in patients without a fourth heart sound (0.56 +/- 0.08 versus 0.71 +/- 0.11, p less than 0.001; 0.46 +/- 0.16 ms-1 versus 0.67 +/- 0.17 ms-1, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Influence of sodium concentration in cerebrospinal fluid on plasma atrial natriuretic peptide in conscious rats.
1. To test the influence of a sodium (Na+) stimulus within the central nervous system on the release of atrial natriuretic peptide (ANP), we examined the effects of intracerebroventricular infusion of high Na+ artificial cerebrospinal fluid (CSF) on blood pressure, urinary Na+ excretion and plasma ANP levels in conscious Wistar rats. 2. Infusion of high Na+ (0.6 mol/l) CSF into the lateral ventricle at a rate of 1 microliter/min for 60 min significantly increased mean blood pressure and urinary Na+ excretion, while normal Na+ (0.15 mol/l) CSF had no effects. Plasma ANP levels were higher in the high Na+ CSF group than in the normal Na+ group (154 +/- 39 vs 52 +/- 19 pmol/l, P less than 0.05). 3. Interruption of the sympathetic nervous system and the vascular action of vasopressin with intravenous hexamethonium and d(CH2)5Tyr(Me)arginine vasopressin attenuated the pressor and natriuretic responses to intracerebroventricular high Na+ CSF. Plasma ANP levels in these rats did not differ significantly from those in rats which were similarly treated but were given normal Na+ CSF. 4. These results indicate that elevation of the CSF Na+ concentration without peripheral volume loading can stimulate ANP release into the circulation. ANP release due to central Na+ stimulus appears to be mediated by the sympathetic nervous system, vasopressin, and/or haemodynamic change caused by these factors.
Animals↗
Antihypertensive drugs and sodium restriction. Analysis of their interaction based on pressure-natriuresis relationship.
The hypotensive effects of some antihypertensive drugs are augmented under sodium restriction, while those of others are not. The mechanisms of these interactions were theoretically analyzed based on the arterial pressure-natriuresis relationship. Four-week studies were performed in 24 patients with essential hypertension who were given a regular sodium diet (12-15 g of NaCl/d) in the first and third weeks and a sodium-restricted diet (1-3 g/d) in the second and fourth weeks. One of three antihypertensive drugs, 60 mg/d of nicardipine (Ca-antagonist), 120 mg/d of propranolol (beta-blocker) or 150 mg/d of captopril (converting-enzyme inhibitor) was administered in the third and fourth weeks. The mean arterial pressure and urinary sodium excretion were measured on the last three days of each week. The degree of interaction between the antihypertensive drugs and sodium restriction was statistically compared. The hypotensive effect of nicardipine and propranolol did not differ with the change in sodium intake, whereas that of captopril was greater under sodium restriction than under the regular sodium diet. Urinary sodium excretion was plotted on the ordinate as a function of arterial pressure before and after administration of the antihypertensive drugs. The pressure-natriuresis curve was shifted left, without a change in the slope, by nicardipine and propranolol and also left, but with a decrease in the slope, by captopril. The hypotensive effect of nicardipine and propranolol, being independent of the amount of sodium intake, was based on the leftward shift of the pressure-natriuresis curve that was probably due to the decrease in renal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
Antihypertensive Agents↗
Cellular mechanism of atrial natriuretic factor secretion by cultured rat cardiocytes.
Using primary culture of atrial cardiocytes from neonatal rats, we have demonstrated that alpha 1-adrenergic and muscarinic cholinergic agonists have a direct stimulatory effect on secretion of atrial natriuretic factor (ANF) and that ANF secretion is stimulated by phorbol ester, Ca2+ ionophore, high K+-induced depolarization and Ca2+-channel agonists. These data suggest that receptor-mediated mobilization of intracellular Ca2+ and activation of protein kinase C as well as Ca2+ influx via voltage-dependent Ca2+ channels are involved in the secretory mechanism of ANF.
Animals↗
Role of calcium and protein kinase C in ANP secretion by cultured rat cardiocytes.
The secretory mechanism of rat atrial natriuretic peptide (rANP) was studied in vitro with the use of primary culture of atrial myocytes from neonatal rats. Norepinephrine, phenylephrine, and carbamylcholine stimulated immunoreactive (IR) rANP secretion, whereas neither angiotensin II, arginine vasopressin, nor isoproterenol affected its secretion. The stimulatory effects of carbamylcholine and phenylephrine were blocked by atropine and prazosin, respectively. 12-O-tetradecanoylphorbol-beta-acetate (TPA), protein kinase C activator, induced a dose-dependent increase in IR rANP secretion, and TPA combined with Ca2+ ionophore ionomycin produced a synergistic effect. Ca2+-channel agonist BAY K 8644 also stimulated IR rANP secretion, the effect of which was blocked by Ca2+-channel antagonist nifedipine. These data suggest that alpha 1-adrenergic and muscarinic cholinergic agonists have direct action on rat cardiocytes to stimulate ANP secretion that involves receptor-mediated mobilization of intracellular Ca2+ and activation of protein kinase C.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Atrial natriuretic peptide, angiotensin, norepinephrine and electrolyte in cerebrospinal fluid of essential hypertension.
We determined concentrations of atrial natriuretic peptide (ANP), angiotensin (Ang), norepinephrine (NE) and electrolyte in plasma and cerebrospinal fluid (CSF) to study possible roles of these substances within the brain in human hypertension. Blood and CSF samples were obtained from 10 patients with mild to moderate essential hypertension (EHT) aged 40-65 y and 10 age-matched normotensive subjects (NT) on a regular salt diet (8 g/day). Levels of ANP, NE, Na, K, Ca and Cl in CSF and plasma were comparable between EHT and NT. Plasma renin activity, plasma and CSF Ang II were lower in EHT than NT. CSF Ang III tended to be lower in EHT. There was no correlation between CSF and plasma ANP, or between CSF and plasma Ang II. Our results indicate that CSF levels of ANP may not be altered in middle aged patients with mild to moderate hypertension. It is also suggested that Ang II, NE and sodium in the central nervous system may not have important roles in hypertension of those patients.
Adult↗
Ventricular myocytes from neonatal rats are more responsive to dexamethasone than atrial myocytes in synthesis of atrial natriuretic peptide.
Using the primary culture of neonatal rat ventricular myocytes, synthesis and secretion of rat atrial natriuretic peptide (rANP) were studied. Ventricular myocytes in culture, although contained less amounts of cellular immunoreactive (IR)-rANP, secreted substantial amounts of IR-rANP at a rate comparable to that of atrial myocytes. Dexamethasone markedly stimulated synthesis and secretion of IR-rANP by cultured ventricular myocytes in a dose-dependent manner (10(-10)-10(-6) M), of which effect was far more potent than that in atrial myocytes. Testosterone and triiodothyronine also stimulated synthesis and secretion of ventricular IR-rANP to the extent comparable to that of atrial IR-rANP. The present study suggests that tissue-dependent difference in glucocorticoids sensitivity plays an important role in the regulation of developmental ANP gene expression in mammalian heart.
Age Factors↗
Atrial natriuretic peptide secretion in mitral stenosis.
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Adult↗
Binding of synthetic beta-human atrial natriuretic peptide to cultured rat vascular smooth muscle cells.
We have studied the effects of synthetic beta-human atrial natriuretic peptide (beta-hANP), an antiparallel dimer of alpha-hANP, on receptor binding and cGMP generation in cultured rat vascular smooth muscle cells and compared the effects with those of alpha-hANP. Characteristics of temperature-dependent binding and degradation of 125I-beta-hANP were similar to those of 125I-alpha-hANP. Scatchard analysis indicated a single class of binding sites for beta-hANP with a maximal binding capacity one-half that of alpha-hANP. Parallel and antiparallel dimers were equipotent in inhibiting the binding and stimulating intracellular cGMP formation, of which the maximal effect was about one-half that of alpha-hANP. Reverse-phase high performance liquid chromatography revealed that most of beta-hANP added to cells was converted to a small molecular mass component corresponding to alpha-hANP after incubation. These data suggest that the less potent effect of beta-hANP in receptor binding and cGMP generation may be partly accounted for by the possible conversion of beta-hANP to alpha-hANP at the site of target cells.
Animals↗