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At least 955 records · Page 53Linked to original sources
PubMed1986

Response of the cardiovascular system to catecholamines in rats given small doses of lead.

Experiments were done in order to assess the influence of low level lead poisoning in rats upon the responses of the rat cardiovascular system to perturbation by norepinephrine, epinephrine, and isoproterenol administration. Wistar rats were given lead acetate (50.0 mg/kg) via stomach tube once weekly for 5 weeks. Control rats were given sodium acetate similarly; both groups of rats were on a regular animal food diet during the experiment. At the end of the sixth week 2 types of responses were determined. Under urethane anesthesia, the response of mean arterial pressure and heart rate in control and lead-poisoned animals to various catecholamines was measured. Also the response of perfusion pressure in isolated mesenteric vessels, to catecholamines, was measured for vessels having been obtained from control and lead poisoned animals. Our results indicate that lead-treated rats, as compared to controls, have augmented and prolonged pressor responses to epinephrine and norepinephrine; less pronounced depression of arterial pressure in response to epinephrine and isoproterenol; and more pronounced tachycardia in response to isoproterenol. In the lead-treated rats, more pronounced vasoconstriction was observed in the perfusion studies upon administration of exogenous norepinephrine. Small doses of lead intensified alpha receptor response, diminished beta receptor response in blood vessels, and increased positive chronotropic action of isoproterenol.

Animals↗
PubMed1988

Effects of nilvadipine on the cardiovascular system in experimental animals.

The effects of 5-isopropyl 3-methyl 2-cyano-1,4-dihydro-6-methyl-4-(m-nitrophenyl)-3,5-pyridinedicarboxylate (nilvadipine, FR 34235, FK 235) on the cardiovascular system were investigated in isolated organs and whole animals. 1. Nilvadipine inhibited Ca2+-induced contractions of isolated dog coronary artery in high-K+, Ca2+-free medium, and the pA2 value was 10.64. In this effect, nilvadipine was 18 times more potent than nifedipine and 525 times more potent than diltiazem. In contrast, its inhibitory effect on Ca2+-induced contractions of isolated guinea pig atria was weaker (pA2:8.2): only twice that of nifedipine and 25 times that of diltiazem. 2. Nilvadipine also inhibited K+-induced 45Ca2+ uptake in isolated dog coronary arteries and isolated guinea pig atria. In the coronary arteries, the IC50 value of nilvadipine was 2.7 x 10(-10) mol/l, which was, respectively 17, 8, and 589 times lower than that of nifedipine, nicardipine and diltiazem. In the atria, on the other hand, the IC50 value of nilvadipine was 4.4 x 10(-9) mol/l, almost the same as that of nifedipine or nicardipine, and 47 times lower than that of diltiazem. These 45Ca2+ uptake inhibitory effects of the drugs were consistent with their effects on mechanical response in both tissues. 3. Nilvadipine (2.6 x 10(-10) mol/l and higher) dose-dependently inhibited ergometrine (ergonovine)-, serotonin-, and norepinephrine-induced contractions of isolated dog coronary artery, and its effects were 2 to 450 times more potent than those of nifedipine, nicardipine and diltiazem. 4. Nilvadipine (2.6 x 10(-8) mol/l or more, 32 micrograms/heart or more), like nifedipine, produced negative inotropic and chronotropic effects in isolated guinea pig atria and in dog heart-lung preparation, and was more potent than nifedipine in the negative chronotropic effect. 5. Nilvadipine in intravenous doses of 1-32 micrograms/kg decreased total peripheral resistance and systemic blood pressure, and slightly increased cardiac output, pulmonary arterial blood flow and stroke volume, but had no significant effects on pulmonary vascular resistance or pulmonary arterial blood pressure. Heart rate decreased at doses of 32 micrograms/kg or more. Nifedipine had almost the same effects as nilvadipine on total peripheral resistance and blood pressure, but was more potent than nilvadipine in increasing effects on cardiac output, stroke volume and pulmonary arterial blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

TGF-beta in the cardiovascular system: molecular mechanisms of a context-specific growth factor.

Transforming growth factor beta-1 is the prototypical member of a class of growth factors whose actions have been strongly implicated in a number of pathophysiologic processes including chronic vascular diseases such as atherosclerosis and hypertension. One of the hall-marks of this class of growth factors is the diverse nature of their actions; a characteristic that is thought to arise from the fact that the effects of these factors are very dependent upon the particular cellular context in which they operate. There has been substantial progress in understanding the molecular signaling mechanisms utilized by these factors. These findings are beginning to provide a mechanistic framework with which to understand the complex and pleiotropic actions of these factors on cells and tissues of the cardiovascular system.

Animals↗
PubMed1990

[Diseases of the cardiovascular system and the function of the endocrine glands in veterans of Soviet Antarctic expeditions].

The authors examined 58 men who had repeatedly participated in the Antarctic expeditions. In addition to a profound study of the cardiovascular system, the insulin tolerance test (0.1 U/kg simple insulin injected by intravenous drip for 90 minutes) was made, permitting the degree of tissue insulin resistance to be quantitatively estimated with measurements of the content of cyclic nucleotides in blood leukocytes and of immunoreactive insulin, C-peptide and counterinsular hormones in the blood before and after the functional test. It was established that with the increase of the number of Antarctic winterings tissue insulin resistance naturally grows regardless of the age of the examinees, manifesting itself in an increase of basal insulinemia, the content of cyclic adenosine monophosphate in blood leukocytes, appreciable increment of insulinemia after infusion of exogenous insulin. Analogous changes were detected in polar researchers suffering from coronary disease, essential hypertension irrespective of the number of winterings. It is concluded that the rise of tissue insulin resistance occurring under the influence of multiple exposures to natural and social factors of high latitudes is a predisposing factor of the formation of cardiovascular pathology.

Adaptation, Physiological↗
PubMed1984

Differential effect of fluorinated analogs of TRH on the cardiovascular system and prolactin release.

The effects of thyrotropin-releasing hormone (TRH) and the TRH-analogs, 4-fluoro-Im-TRH (4-F-TRH) and 2-trifluoromethyl-Im-TRH (2-TFM-TRH), on the cardiovascular system and prolactin (PRL) release were examined in conscious rats. TRH (2.8 or 28 nmol) injected into the anterior hypothalamus produced dose-dependent increments in blood pressure and heart rate; plasma PRL was increased twofold after the higher dose of TRH. 4-F-TRH had effects similar to those of TRH on both the cardiovascular and PRL response. In contrast, the 2-TFM-TRH was significantly less active than TRH or 4-F-TRH in eliciting tachycardia, yet was noticeably more potent in affecting PRL release. These data suggest that the receptors for TRH-induced PRL release may be different from TRH-receptors which mediate central cardiovascular responses.

Animals↗
PubMed1987

Evidence for an antagonism between caffeine and adenosine in the human cardiovascular system.

A randomized, double-blind and placebo-controlled study was performed in 10 normotensive male subjects to analyze a possible antagonism between caffeine and adenosine with respect to their effects on the cardiovascular system in humans. Caffeine alone, 250 mg intravenously (i.v.), increased blood pressure by 9/12 mm Hg, and resulted in a fall of heart rate (HR) of 3 beats/min. Plasma epinephrine (E) rose by 114% after caffeine. Adenosine alone, in an increasing dose of 0.04-0.16 mg/kg/min, induced an increase in systolic blood pressure (SBP) (17 mm Hg), and HR (33 beats/min), a moderate fall in diastolic blood pressure (DBP) (-4 mm Hg), and no change of mean arterial pressure (MAP). At the highest adenosine infusion rate, forearm blood flow, skin temperature (ST), and transcutaneous oxygen tension were lowered, whereas plasma (nor)epinephrine was increased 227.2 and 215.9%, respectively. Adenosine infusion after caffeine induced comparable effects, but the fractional adenosine-induced changes of SBP, HR, plasma catecholamines, plasma renin activity (PRA), and aldosterone all were significantly reduced by previous administration of caffeine. Our results indicate an antagonism between caffeine and adenosine in humans, which may support the suggestion that some circulatory effects of caffeine are caused by an interaction with endogenous adenosine.

Adenosine↗
PubMed2004

Ablation of Ca(v)2.3 / E-type voltage-gated calcium channel results in cardiac arrhythmia and altered autonomic control within the murine cardiovascular system.

Voltage-gated calcium channels are key components in cardiac electrophysiology. We demonstrate that Ca(v)2.3 is expressed in mouse and human heart and that mice lacking the Ca(v)2.3 voltage-gated calcium channel exhibit severe alterations in cardiac function. Amplified cDNA fragments from murine heart and single cardiomyocytes reveal the expression of three different Ca(v)2.3 splice variants. The ablation of Ca(v)2.3 was found to be accompanied by a compensatory upregulation of the Ca(v)3.1 T-type calcium channel, while other voltage-gated calcium channels remained unaffected. Telemetric ECG recordings from Ca(v)2.3 deficient mice displayed subsidiary escape rhythm, altered atrial activation patterns, atrioventricular conduction disturbances and alteration in QRS-morphology. Furthermore, time domain analysis of heart rate variability (HRV) in Ca(v)2.3(-/-) mice exhibited a significant increase in heart rate as well as in the coefficient of variance (CV) compared to control mice. Administration of atropin/propranolol revealed that increased heart rate was due to enhanced sympathetic tonus and that partial decrease of CV in Ca(v)2.3(-/-) mice after autonomic block was in accordance with a complete abolishment of 2(nd) degree atrioventricular block. However, escape rhythms, atrial activation disturbances and QRS-dysmorphology remained unaffected, indicating that these are intrinsic cardiac features in Ca(v)2.3(-/-) mice. We conclude that the expression of Ca(v)2.3 is essential for normal impulse generation and conduction in murine heart.

Animals↗