Cardiovascular system contractility

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. 

It is usually presumed that smooth muscle cells have only one kind of activity, contraction, and that the only alternative to contractile activity is a kind of estivating resting state (Figure 11). The actual situation is of course more complicated. For example, smooth muscles synthesize extracellular filament protein. They also proliferate, particularly in the cardiovascular system. Both of these processes require a considerable amount of control of the cellular economy. 

The most important actions of the (3-blocking drugs are on the cardiovascular system. -Blockers decrease heart rate, myocardial contractility, cardiac output, and conduction velocity within the heart. These effects are most pronounced when sympathetic activity is high or when the heart is stimulated by circulating agonists. 

The effects of phenytoin on the cardiovascular system vary with the dose, the mode and rate of administration, and any cardiovascular pathology. Rapid administration can produce transient hypotension that is the combined result of peripheral vasodilation and depression of myocardial contractility. These effects are due to direct actions of phenytoin on the vascular bed and ventricular myocardium. If large doses are given slowly, dose-related decreases in left ventricular force, rate of force development, and cardiac output can be observed, along with an increase in left ventricular end-diastolic pressure. 

Any implications for the reproductive system arising from an effect on the homeostasis of the major body systems should be considered. For example, compounds that affect the contractility of smooth muscle might be expected to affect the reproductive tract compounds affecting the cardiovascular system might be expected to have an effect in gestation via the maternal circulation or directly on the embryonic cardiovascular system as it develops. 

Cardiovascular system Acetylcholine decreases the contractility (negative inotropy) and decreases the conduction velocity (negative dromotropy) of the atria. It depresses the sinoauricular node, decreases the heart rate (negative chronotropy) and may cause cardiac arrest. 

At doses up to those causing hypnosis, no significant effects on the cardiovascular system are observed in healthy patients. However, in hypovolemic states, heart failure, and other diseases that impair cardiovascular function, normal doses of sedative-hypnotics may cause cardiovascular depression, probably as a result of actions on the medullary vasomotor centers. At toxic doses, myocardial contractility and vascular tone may both be depressed by central and peripheral effects, leading to circulatory collapse. Respiratory and cardiovascular effects are more marked when sedative-hypnotics are given intravenously. 

The hemodynamic effects of compounds supposed to affect the cardiovascular system are evaluated by measuring preload and afterload of the heart, contractility, heart rate, cardiac output and peripheral or coronary flow. To measure these cardiovascular parameters accurately, the use of larger animals such as dogs or pigs is necessary. This experimental model allows the classification of test drugs according to their action as having ... 

The adverse effects of most serious concern relate to the cardiovascular system and seizure threshold. Actions on the adrenergic and cholinergic systems probably contribute to both hypotensive and direct cardiac effects, including alterations in heart rate, quinidine-like delays in conduction, and reduced myocardial contractility. The seizure threshold is lowered, increasing the frequency of epileptic seizures. All of these adverse effects can occur at therapeutic dosages in susceptible populations, such as elderly people, children, and people with cardiac problems or epilepsy, but are also a major cause of morbidity and mortality in accidental or intentional overdosage. Doses in excess of 500 mg can be seriously toxic, and death is fairly common when doses of 2 g or more are taken. 

Toxicity relates to the effects of local anaesthetics on ion channels in excitable membranes in the CNS (producing tingling of the lips, slurred speech, decreased levels of consciousness and seizures) and cardiovascular system (causing arrhythmias and decreased myocardial contractility). 

The function of the cardiovascular system is to maintain adequate tissue perfusion. Cardiac output is the product of heart rate (rhythm) and cardiac contractility (giving rise to stroke volume). These factors are under neuronal, hormonal and mechanical control systems. Pharmacological manipulation of any of these contributors will result in changes in cardiovascular function and hence peripheral blood flow. In human medicine, the primary goal is to increase life expectancy, while maintenance of performance and quality of life are the main priorities in equine medicine. 

Animal studies have detected a variety of pharmacological and biochemical changes in response to chlordimeform exposure. The cause of death following acute exposure appears to be cardiovascular collapse. Chlordimeform interacts directly with and inhibits a2-adrenergic receptors in mammalian systems. Lethal doses of chlordimeform cause decreases in cardiac contractility and peripheral resistance resulting in severe hypotension. Respiratory arrest also occurs but is thought to be secondary to the cardiovascular effects. The effects of chlordimeform on the cardiovascular system share similarities with those seen with local anesthetics such as procaine. Chlordimeform also inhibits monoamine oxidase and acts as an uncoupler of oxidative phosphorylation. 

Cardiovascular System Drugs Affecting Contractility/Rhythm/Circulating... 

Thyroid hormone has multiple effects on the cardiovascular system with various physiological consequences. Several genes that encode important regulatory and structural proteins in the heart have been shown to be thyroid hormone responsive. Thyroid hormone increases cardiac contractility, induces vasorelaxation and angiogenesis, prevents fibrosis and has favorable effects on lipid metabolism (reviewed by Pantos73). 

There are many disorders of the cardiovascular system and blood. Common cardiovascular disorders are cardiac failure, ischaemic heart disease, arrhythmias and hypertension. Although these conditions cannot be cured by drug therapy, there are many drugs available to help control them. Cardiac glycosides are useful in cardiac failure and arrhythmias because they improve myocardial contractility and slow conduction through the heart. 

Penbutolol sulfate is a beta-adrenergic-blocking agent that nonselectively blocks beta-adrenergic receptors, primarily affecting the cardiovascular system (e.g., decreased heart rate, decreased cardiac contractility, decreased BP) and lungs (promotes bronchospasm). It is indicated in the management of mild to moderate hypertension. 

Several types of action on the cardiovascular system will be dealt in here action on the heart (contractile force, automaticity, rythmicity, effect on... 

Cardiovascular System Enflurane causes a concentration-dependent decrease in arterial blood pressure, due, in part, to depression of myocardial contractility and peripheral vasodilation. Enflurane has minimal effects on heart rate. 

Hydralazine (apresoline) causes direct relaxation of arteriolar smooth muscle, possibly secondary to a fall in intracellular Ca concentrations. The drug does not dilate epicardial coronary arteries or relax venous smooth muscle. Hydralazine-induced vasodilation is associated with powerful stimulation of the sympathetic nervous system, likely due to baroreceptor-mediated reflexes, which results in increased heart rate and contractility, increased plasma renin activity, and fluid retention all of these effects counteract the antihypertensive effect of hydralazine. Although most of the sympathetic activity is due to a baroreceptor-mediated reflex, hydralazine may stimulate NE release from sympathetic nerve terminals and augment myocardial contractility directly. Most of hydralazine s effects are confined to the cardiovascular system the decrease in blood pressure after administration is associated with a selective decrease in vascular resistance in the coronary, cerebral, and renal circulations, with a smaller effect in skin and muscle. Because of preferential dilation of arterioles, postural hypotension is not common, and hydralazine lowers blood pressure equally in the supine and upright positions. 

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