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Biomedical subjects

S C Pang

Publications and source records attributed to S C Pang.

At least 91 records · Page 5Linked to original sources
PubMed1990

Decrease of blood pressure in spontaneously hypertensive mice by heat treatment.

Although the increased sensitivity of hypertensive animals to heat stress has been reported, the effect of chronic heat exposure has not been examined. The specific goal of the present investigation was to study the impact of chronic heat treatment on the blood pressure of spontaneously hypertensive mice. Chronic 40 degrees C heat exposure for 5 min daily progressively lowered basal blood pressure in hypertensive mice within 20 days, without any change in normal mice. In fact, after 35 days of chronic heat treatment, the basal blood pressure of hypertensive mice was indistinguishable from that of the normotensives. Repeated immobilization and prewarming as normal procedures for recording blood pressure contributed to the decrease in blood pressure by 10 to 12 mm Hg, but chronic heat by itself was significantly more potent in reducing it by an additional 20 mm Hg. After the discontinuation of chronic heat application, the basal blood pressure of hypertensive mice returned with time to the level registered in sham-handled hypertensive controls. These results demonstrate that, although acute heat is more detrimental to hypertensive mice, brief, chronic exposure to mild heat stress is beneficial in that it normalizes basal blood pressure.

Animals↗
PubMed1989

Atrial natriuretic factor-induced egression of cyclic guanosine 3':5'-monophosphate in cultured vascular smooth muscle and endothelial cells.

The induction of cyclic GMP formation in target tissues, i.e. vascular smooth muscle and endothelial cells, by atrial natriuretic factor is followed by its egression into plasma and urine. Since the extracellular appearance of this cyclic nucleotide is used as a marker of atrial natriuretic factor's biological activity, the present study was designed to investigate the characteristics of its egression to the extracellular fluid. In contrast to cyclic AMP, whose profile of egression in time closely follows its intracellular levels, cyclic GMP egression begins with the intracellular decline but continues for a prolonged period, even accumulating for up to 24 h in the extracellular medium. The relative egression of cyclic GMP decreases slightly in the presence of phosphodiesterase inhibitors. On the other hand, the process is sensitive to temperature, inhibited by such agents as probenecid, and occurs against a gradient of 7 orders of magnitude. Large increases of cyclic AMP, as induced by forskolin, can effectively compete for the cyclic GMP transport system, resulting in a 3-fold rise in intracellular cyclic GMP levels, which corresponds to a 3-fold decline of extracellular accumulation. Although the biological significance of cyclic GMP egression is unknown, the results of this study suggest that the process may be one of the significant contributors to the control of cyclic GMP levels in the cell with potential physiological consequences.

Animals↗
PubMed1989

In vitro proliferation of aortic smooth muscle cells from spontaneously hypertensive and normotensive rats.

The characteristics and proliferation of aortic smooth muscle cells (SMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were studied in culture. Smooth muscle cells were isolated from the tunica media of the thoracic aorta by an explant method. Immunofluorescence microscopy showed that 93-95 per cent of cells were positively labelled with antibodies raised against smooth muscle actin, indicating that these were smooth muscle cells. The proliferative activity was compared between aortic smooth muscle cells from hypertensive and normotensive rats in culture by thymidine incorporation and cell number determinations. The results demonstrate that aortic smooth muscle cells from hypertensive rats grew faster than those from normotensive rats in culture. The increased proliferative activity of cultured aortic smooth muscle cells from hypertensive rats was detectable even when they were cultured in a chemically defined serum-free medium. These data have shown that an increased proliferative activity of aortic smooth muscle cells from hypertensive rats can occur in culture conditions without the influence of arterial pressure or other stimuli as in intact animals. The mechanisms underlying the accelerated proliferative activity of aortic smooth muscle cells from genetically hypertensive rats in vitro remain to be determined.

Animals↗
PubMed1989

Effect of atrial natriuretic factor on blood-brain barrier permeability.

Recent studies have demonstrated receptors for atrial natriuretic factor on endothelium of intracerebral vessels. The physiological role of these receptors is not known. The present study was undertaken to determine whether atrial natriuretic factor has an effect on blood-brain barrier permeability to protein and ions using horseradish peroxidase and lanthanum as markers of permeability alterations. This study does not demonstrate a significant effect of atrial natriuretic factor on blood-brain barrier permeability mechanisms in steady states.

Animals↗
PubMed1989

Ultrastructure of atrial and ventricular myocytes of newborn rats: evidence for the existence of specific atrial granule-like organelles in the ventricle.

The present study examined the ultrastructure of atrial and ventricular myocytes from the heart of newborn rats. It was found that, despite former reports stating that ventricular myocytes in adults do not contain cytoplasmic granules, specific atrial granule-like organelles are present in the ventricles of rats at birth. The presence of these granules together with the relatively underdeveloped contractile apparatus and extensive Golgi complex suggests that the ventricular, like the atrial, myocytes may have an endocrine function before or at birth. Further study is required to determine whether these ventricular cytoplasmic granules contain the same atrial natriuretic peptide species known to be present in the atrial specific granules.

Animals↗
PubMed1988

Atrial natriuretic peptide during supraventricular tachycardia and relation to hemodynamic changes and renal function.

Changes in plasma levels of atrial natriuretic peptide (ANP) and arginine vasopressin were studied in 5 patients during and after a 30-minute period of induced supraventricular tachycardia (SVT). Immediately after the induction of SVT, plasma ANP levels began to increase, peaked at 32 minutes (+734% increase on average) and then gradually decreased. The mean plasma arginine vasopressin levels decreased during SVT, but the differences were not significant. When plasma ANP levels during SVT were compared with the simultaneously measured hemodynamic variables, a significant positive correlation (r = 0.73, p less than 0.001) was observed between plasma ANP levels and pulmonary capillary wedge pressure. Induced SVT was associated with increased urinary sodium and potassium excretion, increased urine flow and increased free water clearance. Concomitantly, glomerular filtration rate significantly increased (+77%) with an increase in filtration fraction. Although no significant change was observed in plasma renin activity, plasma aldosterone concentrations decreased during and after SVT. These results suggest that increased left atrial pressure stimulates ANP release during SVT and that increased glomerular filtration rate and decreased aldosterone secretion by ANP, in addition to the inhibition of water reabsorption by decreased arginine vasopressin, may be responsible for natriuresis and diuresis associated with SVT.

Adult↗
PubMed1988

Abnormality of calmodulin activity in hypertension. Evidence of the presence of an activator.

An apparent increase of calmodulin (CaM) activity was previously observed in the heart and kidney but not in the liver of spontaneously-hypertensive rats (SHR) and mice compared with their corresponding normotensive controls. As this change was due to an elevated recovery of CaM in the organs of the hypertensive animals, the present study was designed to evaluate its activity in hypertension. A CaM activator, detected in heart and kidney supernatants from hypertensive animals, was found to be responsible for this enhanced recovery. Similar results were obtained with passaged, cultured aortic smooth muscle cells from SHR, indicating that the anomaly was not a mere consequence of elevated blood pressure but rather a genetic expression of cells of hypertensive origin. The activator was heat stable, nondialyzable, and recovered in the fraction precipitated with 30-50% ammonium sulfate. Preliminary extraction studies suggest that the activator is contained in a glycolipid fraction. The stimulation of phosphodiesterase by this activator was calcium and CaM dependent. The activator appears to affect the affinity of the phosphodiesterase for CaM rather than the maximal stimulation. The activator was also present at a low concentration in the heart and kidney of normotensive animals. These findings indicate that at least some of the calcium abnormalities implicated in the pathogenesis of hypertension could be the result of interactions between CaM, calcium, and this activator.

Animals↗
PubMed1988

Early diagnosis of acute myocardial infarction by myoglobin latex agglutination test.

Early elevation of the serum myoglobin level in acute myocardial infarction (AMI) has been noted for years. In this study, 39 patients admitted to the Coronary Care Unit with acute chest pain within 72 hours (mean 12 +/- 15 hours) or electrocardiographic changes suspected of acute myocardial infarction had a serum myoglobin latex agglutination test to evaluate its diagnostic accuracy in acute myocardial infarction. Of these 39 patients, 24 had documented acute myocardial infarction as their final diagnosis. By the time of admission, 18 of the 24 cases with infarction had positive myoglobin tests (sensitivity 75%). Of those 15 cases without myocardial infarction, 13 had negative myoglobin tests (specificity 87%). If only those 17 cases admitted within 5 hours of the onset of chest pain were analyzed, the serum myoglobin test became positive in 8 of 10 cases with documented AMI but the 2 cases with negative results turned positive 2 hours later (sensitivity 80% to 100%). Due to the fact that myoglobin tests were negative in all other 7 cases without infarction, the specificity was 7/7 (100%). In contrast, the creatine phosphokinase isoenzyme study was positive only in 3 of these 10 patients with documented AMI in the first blood sample taken during admission. In conclusion, the serum myoglobin latex agglutination test is a quick and reliable method that helps in the early diagnosis of acute myocardial infarction.

Adult↗
PubMed1987

Cardiac and renal hyperplasia in newborn spontaneously hypertensive rats.

Cardiac hyperplasia in newborn spontaneously hypertensive rats (SHR) has been noted by our group as well as by other investigators. The present study was designed to establish whether early (neonatal) hyperplasia is confined to the heart or is a generalized phenomenon in this hypertensive model. The ventricles, kidney and liver of newborn SHR, Wistar and Wistar-Kyoto (WKY) rats were analysed for their protein and DNA content. Total organ weight and the organ/body weight ratio of the heart and kidney but not of the liver were significantly greater in the SHR than in the control rats, irrespective of total body weight. The higher relative DNA content (per 100 mg of tissue or 100 g body weight) indicated that hyperplasia rather than hypertrophy was responsible for the enlarged heart as well as the kidney of newborn SHR. The cause of this selective cardiac and renal hyperplasia is not yet known: it may be due to putative 'haemodynamic growth stimuli', an intrinsic genetic abnormality of cells in the heart and kidney, circulating growth-promoting factors, or innervation.

Animals↗
PubMed1987

Diagnostic accuracy of two-dimensional echocardiography for detection of left atrial thrombus in patients with mitral stenosis.

Two-dimensional echocardiograms of 56 patients with mitral stenosis, who subsequently underwent operation, were analyzed to evaluate the accuracy for the detection of left atrial thrombi. From left parasternal, apical, and subcostal cardiac windows, multiple planes (including standard planes and their derived scanning planes) were assessed for the presence or absence of mass echoes in the left atrium. The results showed 63% sensitivity, 95% specificity, 87% positive predictive value, 84% negative predictive value, and 83% overall diagnostic accuracy. Most of the false-negative cases had their thrombi confined to the left atrial appendage. We conclude that in patients with mitral stenosis, two-dimensional echocardiography is promising for the diagnosis of left atrial thrombi, particularly when they locate or extend to the main left atrial cavity (not confined to atrial appendage).

Adult↗
PubMed1986

ANF stimulation of detergent-dispersed particulate guanylate cyclase from bovine adrenal cortex.

Particulate guanylate cyclase from bovine adrenal cortex can be stimulated by ANF. A 2-fold stimulation of the enzyme was obtained with 100 nM ANF and a half-maximal stimulation, with a 5 nM dose. The stimulation by ANF persisted for at least 30 min. Various detergents, such as Triton X-100, Lubrol PX, cholate, CHAPS, digitonin and zwittergent, stimulated several-fold the activity of particulate guanylate cyclase. However, only Triton X-100 dispersed particulate guanylate cyclase without affecting its response to ANF. The dose-response curve of ANF stimulation of the particulate and the Triton X-100 dispersed enzyme was similar. The dispersion of a fully responsive guanylate cyclase to ANF will help us to uncover the type of interactions between guanylate cyclase and ANF. It will also be used as a first step for the purification of an ANF-sensitive particulate guanylate cyclase.

Adrenal Cortex↗
PubMed1986

Cyclic GMP as mediator and biological marker of atrial natriuretic factor.

Both our previous and the present studies established that increases in cyclic guanosine monophosphate (cGMP) reflect the activity of atrial natriuretic factor (ANF). The ANF message is transmitted by particulate guanylate cyclase, which appears to be in intimate contact with the ANF receptor since stimulation of particulate guanylate cyclase is observed even after dispersion of the membranes. The stimulation of smooth muscle and endothelial cells in culture leads to egression of cGMP to extracellular medium where it accumulates for over 2 h. The signal of the extracellular cGMP is magnified and prolonged compared to the intracellular signal. The stimulation of cGMP production by ANF in vascular smooth muscle and endothelial cells appears to be relatively irreversible and the responsiveness is down-regulated by prior exposure to low doses of ANF. Cyclic guanosine monophosphate can also serve as a marker for ANF action. Atrial natriuretic factor fragments of different potencies exert a biological activity that correlates with ANF-induced cGMP increases. In hypertensive rats and monkeys, where acute infusion of ANF leads to an exaggerated diuresis and natriuresis, urinary cGMP does not appear to be different. Overall, cGMP appears to be a mediator and a marker of ANF biological activity and may serve as a useful tool in the study of pathogenesis of hypertension.

Animals↗
PubMed1986

Cardiac and renal hyperplasia in newborn genetically hypertensive rats.

Newborn spontaneously hypertensive rats (SHR), compared with Wistar-Kyoto (WKY) controls, usually show cardiac and renal hyperplasia. To determine whether these anomalies are common to genetically hypertensive rats, we examined newborn rats from models of essential hypertension (Kyoto, Montreal, Dunedin and Lyon strains of hypertensive rats), renal hypertension (Milan strain of hypertensive rats) and experimental hypertension [deoxycorticosterone acetate (DOCA)-salt hypertensive Wistar rats]. The hearts, kidneys and livers of these newborns were collected on site at various centres and sent to Montreal for protein and DNA determinations. The results showed that protein and DNA, corrected for body weight in models of essential hypertension, were increased in the heart and kidney, and normal or decreased in the liver at birth. This pattern differed in offspring of the Milan strain (renal hypertension) and of DOCA-salt hypertensive animals (experimental hypertension). Since cardiac and renal hyperplasia associated with the hypertensive trait in four different genetic models of spontaneous hypertension was distinct from that observed in renal and experimental hypertension, it is conceivable that a specific cardiovascular growth pattern is a reflection not of a simple linkage or consequence, but of a causal association with spontaneous hypertension.

Animals↗
PubMed1985

The increase of cGMP by atrial natriuretic factor correlates with the distribution of particulate guanylate cyclase.

We have demonstrated previously that atrial natriuretic factor (ANF) augments urinary, plasma and kidney cGMP levels but has no significant effect upon cAMP. Using cGMP as a marker, we searched for specific target sites involved in the action of ANF in the dog kidney, and observed no change of cGMP in the proximal tubules, a 2-fold increase over basal levels in the thick loop of Henle and a 3-fold elevation in the collecting duct. The most striking action on cGMP occurred in the glomeruli with a rise of up to 50-fold being evident at 1-2 min. after the addition of ANF. The results obtained in the absence or presence of a phosphodiesterase inhibitor support the notion that the effects of ANF were exerted at the level of guanylate cyclase stimulation rather than cGMP phosphodiesterase inhibition. The action of sodium nitroprusside (SNP), a direct stimulator of soluble guanylate cyclase, differed from that of ANF. The ability of the factor to enhance cGMP levels was correlated with the distribution of particulate guanylate cyclase. This study identifies the glomeruli and the distal part of the nephron as specific targets of ANF and implicates particulate guanylate cyclase as the enzyme targetted for the expression of its action.

Animals↗
PubMed1985

Effect of natural and synthetic atrial natriuretic factor on arterial blood pressure, natriuresis and cyclic GMP excretion in spontaneously hypertensive rats.

The differential effects of extracted and synthetic atrial natriuretic factor (ANF) on arterial blood pressure, natriuresis, and cyclic GMP excretion were studied in normotensive (WKY) and spontaneously hypertensive (SHR and SHRSP) rats. Atrial extracts or synthetic (101-126)-ANF decreased arterial blood pressure in all tested animals, but the blood pressure-lowering effect was more pronounced in hypertensive than in normotensive rats. ANF-induced diuresis and natriuresis were two- to three-fold higher in the hypertensive groups. However, a several-fold increase in total urinary cyclic GMP level after the infusion of ANF was essentially equal in the three groups. Our data suggest that acute infusion of ANF reveals a defect of sodium and water handling in SHR. It is possible that this defect is located at the distal nephron, and is made apparent by the action of ANF on glomeruli via a cyclic GMP-induced vascular effect.

Animals↗
PubMed1985

Primary versus secondary events in hypertension.

Functional modifications, such as a reduction in hormonal response, which occur in the cardiovascular system in hypertension, are reflected at the cellular level by anomalies in cyclic nucleotide and other messenger systems. To distinguish between primary and adaptive abnormalities, we pursued three research strategies. (i) Investigations on various models of hypertension. To be considered a primary defect, an abnormality should also be present in other genetically hypertensive models. Indeed, we have confirmed the occurrence of cellular hyperplasia in the heart of spontaneously hypertensive rats (SHR) as well as in spontaneously hypertensive mice (SHM). An increase of calmodulin levels in the heart and kidney is also observed in both the SHR and SHM. (ii) Studies on the evolution of hypertension with age. In humans, a decrease of cAMP levels in response to beta-adrenergic stimulation in older patients is contrasted with an excess in younger subjects. In the SHR, protein kinase activity of the heart is lower in the prehypertensive stages, whereas this defect appears much later in the aorta. (iii) Experiments on anomalies in newborns and cultured cells. The heart and kidney in the SHR exhibit significant hyperplasia at birth, and an abnormal growth continues in tissue culture. We hope that these strategies will eventually help to provide biochemical and functional markers for genetic analysis of factors which may be involved in the pathogenesis of hypertension.

Aging↗
PubMed1985

An examination of the arterial media in transplanted arteries of spontaneously hypertensive (SHR) and normotensive Wistar Kyoto rats (WKY).

The hypothesis that arterial medial hypertrophy occurs in the SHR due to genetic factors inherent to the arterial wall, was examined in jejunal arteries cross transplanted between four-week-old SHR and WKY rats as a shunt between the femoral artery and vein. Four weeks after transplant, the arteries were removed and processed for embedding in resin and measurement of wall parameters by light microscopy. It was determined that irrespective of the origin of the transplanted artery, the wall thickness of transplants was higher in SHR hosts than in WKY hosts. Taken with results from other studies, this suggests that genetic factors inherent to the arterial wall are not the cause of arterial hypertrophy in the SHR.

Animals↗