Department of Physiology, School of Medicine, GMU
Maintenance of the internal environment in the body (maintaining the optimum biochemical environment).
Hipophysis posterior hormone
Anti diuretic hormone or VASOPRESSIN
Stimulate the contraction of smooth muscle in the arterioles, small blood vessels that connect the arteries to capilleries
as a result of ADH , blood vessels constrict, and blood pressure rises
Oxytocin
It has long been known that OT induces natriuresis and causes a fall in mean arterial pressure, both after acute and chronic treatment, but the mechanism was not clear
oxytocin triggers ANP release in vivo
HYPOFISIS ANTEROR HORMONE
GROWTH HORMONE AND CV
The physiological nature of cardiac growth is accounted for by the following: (i) the increment in cardiomyocyte size occurs prevalently at expense of the short axis. This is the basis for the concentric pattern of left ventricular (LV) hypertrophy, with consequent fall in LV wall stress and functional improvement; (ii) cardiomyocyte growth is associated with improved contractility and relaxation, and a favourable energetic setting; (iii) the capillary density of the myocardial tissue is not affected
(iv) there is a balanced growth of cardiomyocytes and nonmyocyte elements, which accounts for the lack of interstitial fibrosis; (v) myocardial energetics and mechanics are not perturbed; and (vi) the growth response is not associated with the gene re-programming that characterizes pathologic cardiac hypertrophy and heart failure
interaction of GH with the cardiovascular system accounts for: (i) the lack of cardiac impairment in short-term acromegaly; (ii) the beneficial effects of GH and IGF-I in various models of heart failure; (iii) the protective effect of GH and IGF-I against post-infarction ventricular remodelling; (iv) the reversal of endothelial dysfunction in patients with heart failure treated with GH; and (v) the cardiac abnormalities associated with GH deficiency and their correction after GH therapy
GH, through its nitric oxide (NO)-releasing action, contributes to the maintenance of normal vascular reactivity and peripheral vascular resistance
Prolactin
PRL-releasing peptide (PrRP) is a hypothalamus peptide that stimulate prolactin production
Noradrenaline (NA) and PRL-releasing peptide (PrRP) that are produced by these neurons will stimulate the release of ACTH from the anterior pituitari through the CRH hypothalamic neurons
The effects of intravenous infusions of prolactin on the arterial pressures of decerebrate rabbits were studied
The increasing of arterial pressure is prolactin administration dose dependent
Other gland
GLUCOCORTICOID AND CV :
Maintenance of normal circulatory function
Essential for the maintenance of normal myocardial contractility and vascular resistance
Their action on the vasculature is a permisive one in that they potentiate the vasoconstrictor effect of catecholamines
Also decrease the permeability of vascular endothelium and therefore maintain blood volume
CATECHOLAMINES AND CV :
Their action are depend on their binding to various adrenoceptor (a and b adrenoceptor )
Noradrenalin cause wide spread vasocontriction and a marked increase in peripheral resistance
Adrenaline causes vasoconstriction in skin and viscera but vasodilatation in skletal muscle so that total peripheral resistance may decrease
Both catecholamines increase heart rate and contractility directly
Noradrenaline administration leads to reflex bradycardia
INSULIN :
insulin and leptin cooperate in the modulation of vascular tone through enhancement of endothelial NO release. A major impact on the regulation of the cardiovascular system, principally in those clinical conditions characterized by endothelial NO dysfunction and metabolic disorders, such as arterial hypertension.
Changes in cardiohemodynamics after i.v of insulin (1.0 IU/kg) were investigated on dogs. During the first 5-10 min (phase 1 of the response), coronary vasoconstriction, an enhancement of the cardiac activity and an increase in a coronary arteriovenous oxygen difference were observed. During the next 25-30 min (phase II) a long-term coronary dilation, an attenuation of the cardiac contractility and a decrease in the coronary arteriovenous oxygen difference occurred.
the post-prandial state is accompanied by endothelial dysfunction in Type 2 diabetic patients and that insulin as apart improved endothelial function.
Insulin resistance represents a common metabolic abnormality leading to cardiovascular disease
Increased plasma plasminogen activator inhibitor 1 (PAI-1) levels were associated with insulin resistance and atherothrombosis added for the first time a pathological basis for an association of the insulin resistance syndrome not only with metabolic, atheromatous (atherosclerotic) risk but also with atherothrombotic risk. It is very likely that not only PAI-1, but also other abnormalities in haemostatic variables contribute to this excess vascular risk.
Insulin resistance is a key factor in the pathogenesis of type 2 diabetes, and it predates the development of frank hyperglycemia by many years. Characteristic features of the insulin resistance syndrome include dyslipidemia, glucose intolerance, central obesity, hypertension, and specific abnormalities of endothelial and vascular function. The interplay between these signs of insulin resistance and their vascular, metabolic, and clinical consequences points to increased risks of CVD and type 2 diabetes
SEX HORMONE AND CV :
The greater incidence of hypertension and coronary artery disease in men and postmenopausal women compared with premenopausal women has been related, in part, to gender differences in vascular tone and possible vascular protective effects of the female sex hormones estrogen and progesterone
Estrogen, progesterone, and testosterone receptors have been identified in blood vessels of human and other mammals and have been localized in the plasmalemma, cytosol, and nuclear compartments of various vascular cells, including the endothelium and the smooth muscle.
The sex hormone-induced stimulation of the endothelium-dependent mechanisms of vascular relaxation and inhibition of the mechanisms of vascular smooth muscle contraction
ESTROGEN AND CV :
Inflammation plays an important role in the response to endoluminal vascular injury. Estrogen (17beta-estradiol, E2) inhibits neointima formation in animal models
E2 may limit the neointimal response to endoluminal vascular injury, at least in part, by limiting leukocyte entry from adventitial/periadventitial tissues into injured vessels early in the injury response.
Estrogen also has anti-clot functionAvoid the formation of thrombus and thus can slow down the hardening of arteries
Microvascular endothelial cells -- cells in the lining of the smallest blood vessels -- produce estrogen and express estrogen receptor
Blood clots are occasional but serious side effects of estrogen therapy.
They are dose-related, that is, they occur more frequently with higher doses of estrogen
Estrogen may derive part of its known cardiovascular protective effect by increasing production of nitric oxide in microvascular endothelial cells
Decreasing of Estrogen may induce arythmia
P and CV
postmenopausal women, higher blood levels of progesterone are associated with less of an increase in blood pressure and less blood vessel constriction in response to angiotensin II, one of the naturally occurring substances in the body which causes the blood vessels to constrict
postmenopausal women, higher blood levels of progesterone are associated with less of an increase in blood pressure and less blood vessel constriction in response to angiotensin II, one of the naturally occurring substances in the body which causes the blood vessels to constrict
TESTOSTERONE AND CV :
Male sex is an acknowledged risk factor for many forms of cardiovascular disease, and vascular disease prevalence patterns appear to be different in men versus women. The vascular properties of the principal mammalian androgen, testosterone, are complex and linked to dose, duration of exposure, presence of underlying vascular disease, and, possibly, biological sex
lower levels of testosterone in men are associated with higher blood pressure, left ventricular mass, and left ventricular hypertrophy.
Data from isolated vessels and animal models suggest that pharmacological doses of testosterone, or its potent intracellular metabolite dihydrotestosterone, produce vasodilation.
Testosterone's major effect on vascular beds at physiologic concentrations remains unclear, with documentation of both vasodilatory and vasoconstrictive actions
Results of various studies suggest that testosterone can alter vascular tone through both endothelium-dependent and endothelium-independent mechanisms in a variety of vascular beds and vessel types
Testosterone's endothelium-dependent effects are likely mediated at least in part through nitric oxide (NO) elaboration, whereas mechanisms of endothelium-independent effects involve 1 or more types of smooth muscle ion conductance channels
Clinical studies indicate that, in men, androgen replacement may provide beneficial effects when coronary artery disease is present
High-dose testosterone significantly increased the circulating plasma testosterone concentration, and was associated with a dramatic increase in brachial artery vasodilatation
Direct infusion of physiological concentrations of testosterone into the right coronary artery of men with CAD is reported to increase coronary artery diameter and coronary blood flow consistent with a direct vasodilatory activity
In contrast, clinical studies conducted in hypogonadal men demonstrate a neutral influence of testosterone replacement upon vascular reactivity.
Males with CAD and associated low serum levels of testosterone, is the population in which testosterone replacement therapy may be clinically advantageous
in women, testosterone may augment existing hypertension, increase risk for cardiovascular events, or promote atherogenesis.
there is a relationship between endogenous androgen levels and arterial stiffness in older men.
THYROID HORMONE AND CV :
Thyroid state plays an essential role in the development of membrane phospholipid components in cardiac membranes during the early postnatal period.
Hypothyroidism patients have increased cardiovascular risk, although the mechanism is not defined.
Thyroid have chronotropic effect (increase number and affinity of b adrenergic receptors) and inotropic effect (enhance response to circulating catecholamines and increase proportion of a myosin heavy chain) on the heart as a target tissue
Endothelial dysfunction may initiate atherosclerosis, is present in patients with hypothyroidism, and therefore may link hypothyroidism and vascular disease.
hypothyroidism causes changes in such parameters of cardiovascular function as heart rate, left ventricular systolic and diastolic function, blood, arterial pressure and systemic vascular resistance.
In hyperthyroid CO is increased, peripheral vascular resistance is lower, heart rate and pulse pressure is increased, tachycardia.
Myocardial calcium uptake is increased in thyrotoxic rats
Long standing hyperthyroidism may lead to cardiomegaly and a "high output" congestive heart failure
Minor endocrine gland
Atriopeptin (atrialnatritic factor)
Helps maintain homoestatic balance of fluids, electrolytes.
Lowers blood pressure, blood volume
Target areas are blood vessel, kidneys and adrenal glands
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