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J-shaped growth curve A curve on a graph that records the situation in which, in a new environment, the population density of an organism increases rapidly in an exponential (logarithmic) form, but then stops abruptly as environmental resistance (e.g. seasonality) or some other factor (e.g. the end of the breeding phase) suddenly becomes effective. It may be summarized mathematically as: dN/dT = r (with a definite limit on N) where N is the number of individuals in the population, T is time, and
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  J-shaped growth curve A curve on a graph that records the situation in which, in a new environment,the population density of an organism increases rapidly in an exponential (logarithmic) form, but then stops abruptly as environmental resistance (e.g. seasonality) or some other factor (e.g. the end of thebreeding phase) suddenly becomes effective . It may be summarized mathematically as: dN/dT = r (witha definite limit on N) where N is the number of individuals in the population, T is time, and r is aconstant representing the biotic potential of the organism concerned. Population numbers typically show great fluctuation, giving the characteristic ‘boom and bust’ cycles of some insects, or as seen in algal blooms. This type of population growth is terme d ‘density - independent’ as the regulation of  growth rate is not tied to the population density until the final crash. The L-arginine pathway within endothelial cells in the blood vessel wall is the source of production of the endogenous nitrovasodilator, nitric oxide (NO) . NO is released under basal conditions and inresponse to various stimuli such as shear stress and in response to platelet-derived products,coagulation factors and hormones. NO is the mediator of endothelium-dependent relaxation in thecirculation and exerts its effects by activating soluble guanylyl cyclase in vascular smooth muscle,which in turn leads to the formation of cyclic guanosine monophosphate (cGMP) and to relaxation. Inaddition to its effects on vascular smooth muscle, NO is also released abluminally to interact withcirculating platelets. Increases in cGMP in platelets are associated with a decreased adhesion andaggregation of cells. Thus , endothelium-derived NO, through its vasodilator and anti-aggregatoryproperties, prevents vasospasm and thrombus formation in the circulation and thereby helps tomaintain blood flow to vital organs such as the heart.Enzim yang mengubah angiotensin I menjadi angiotensin II disebut dengan Angiotensin ConvertingEnzyme (ACEHigh blood pressure can be divided into two major categories. When high blood pressure occurswithout apparent cause, it is known as primary or essential hypertension; and when it occurs becauseof another disease, such as poor kidney function, it is known as secondary hypertension.There are several different types of drugs that are used to treat hypertension. These include diuretics,which act by forcing the kidneys to excrete water and sodium at a faster rate; and beta blockers,which lower heart rate and cardiac output. Other drugs known as ACE inhibitors affect the levels of hormones that constrict blood vessels.Another major class of drugs used to lower high blood pressure blocks the channels which transportcalcium across muscle cell membranes.  Pheochromocytoma is a rare catecholamine-secreting tumor derived from chromaffin cells. Tumorsthat arise outside the adrenal gland are termed extra-adrenal pheochromocytomas orparagangliomas. Because of excessive catecholamine secretion, pheochromocytomas may precipitatelife-threatening hypertension or cardiac arrhythmiasThe clinical manifestations of a pheochromocytoma result from excessive catecholamine secretion bythe tumor. Catecholamines typically secreted, either intermittently or continuously, includenorepinephrine and epinephrine; rarely, dopamine is secreted. The biological effects of catecholamines are well known. Stimulation of alpha-adrenergic receptors results in elevated bloodpressure, increased cardiac contractility, glycogenolysis, gluconeogenesis, and intestinal relaxation.Stimulation of beta-adrenergic receptors results in an increase in heart rate and contractility.Many cardiac manifestations are associated with pheochromocytomas. Hypertension is the mostcommon complication. Cardiac arrhythmias, such as atrial and ventricular fibrillation, may occurbecause of excessive plasma catecholamine levels. Other complications include myocarditis, signs andsymptoms of myocardial infarction,3 dilated cardiomyopathy, and pulmonary edema, either of cardiac or noncardiac srcinThe pulse rate of patients after application of racemic epinephrine-impregnated retraction cordsdepends more on the level of anxiety and stress than on the level of the epinephrine. Blood pressureis elevated by placement of racemic epinephrine-impregnated retraction cords upon an exposedvascular bed or lacerated tissue.Stress can cause hypertension through repeated blood pressure elevations as well as by stimulation of the nervous system to produce large amounts of vasoconstricting hormones that increase bloodpressureA normal amount of circulating water within the body helps to maintain normal blood pressure in theblood vessels, as well as regulate overall body temperature and other functions. However, when toomuch sodium is ingested it can cause the body to retain more water than necessary.This hoarding of excess water by the body, and its continued movement through the body causesblood pressure to increase inside blood vessel walls, according to the Colorado State UniversityACE inhibitors produce vasodilation by inhibiting the formation of angiotensin II. This vasoconstrictoris formed by the proteolytic action of renin (released by the kidneys) acting on circulatingangiotensinogen to form angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensinconverting enzyme.  ACE inhibitors have the following actions:* Dilate arteries and veins by blocking angiotensin II formation and inhibiting bradykininmetabolism. This vasodilation reduces arterial pressure, preload and afterload on the heart.* Down regulate sympathetic adrenergic activity by blocking the facilitating effects of angiotensin IIon sympathetic nerve release and reuptake of norepinephrine.* Promote renal excretion of sodium and water (natriuretic and diuretic effects) by blocking theeffects of angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosteronesecretion. This reduces blood volume, venous pressure and arterial pressure.* Inhibit cardiac and vascular remodeling associated with chronic hypertension, heart failure, andmyocardial infarction.ACE inhibitors are effective in the treatment of primary hypertension and hypertension caused byrenal artery stenosis, which causes renin-dependent hypertension owing to the increased release of renin by the kidneys. Reducing angiotensin II formation leads to arterial and venous dilation, whichreduces arterial and venous pressures. By reducing the effects of angiotensin II on the kidney, ACEinhibitors cause natriuresis and diuresis, which decreases blood volume and cardiac output, therebylowering arterial pressure.contoh ACE inhibitor: kaptopril
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