Arteries blood pressure

Hypertension is one of the two principal risk factors of many cardiovascular diseases, such as coronary heart disease (CHD), stroke, and CHF. Individuals are considered hypertensive if their systoHc arterial blood pressure is over 140 mm Hg (18.7 Pa) or their diastoHc arterial blood pressure is over 90 mm Hg (12 Pa). Over 60 million people, or one-third of the adult population in the United States are estimated to be hypertensive (163). About 90% of these patients are classified as primary or essential hypertensive because the etiology of their hypertension is unknown. It is generally agreed that there is a very strong genetic or hereditary component to this disease. 

It is well accepted that hypertension is a multifactorial disease. Only about 10% of the hypertensive patients have secondary hypertension for which causes, ie, partial coarctation of the renal artery, pheochromacytoma, aldosteronism, hormonal imbalances, etc, are known. The hallmark of hypertension is an abnormally elevated total peripheral resistance. In most patients hypertension produces no serious symptoms particularly in the early phase of the disease. This is why hypertension is called a silent killer. However, prolonged suffering of high arterial blood pressure leads to end organ damage, causing stroke, myocardial infarction, and heart failure, etc. Adequate treatment of hypertension has been proven to decrease the incidence of cardiovascular morbidity and mortaUty and therefore prolong life (176—183). 

P-Adrenoceptor Blockers. There is no satisfactory mechanism to explain the antihypertensive activity of P-adrenoceptor blockers (see Table 1) in humans particularly after chronic treatment (228,231—233). Reductions in heart rate correlate well with decreases in blood pressure and this may be an important mechanism. Other proposed mechanisms include reduction in PRA, reduction in cardiac output, and a central action. However, pindolol produces an antihypertensive effect without lowering PRA. In long-term treatment, the cardiac output is restored despite the decrease in arterial blood pressure and total peripheral resistance. Atenolol (Table 1), which does not penetrate into the brain is an efficacious antihypertensive agent. In short-term treatment, the blood flow to most organs (except the brain) is reduced and the total peripheral resistance may increase. 

Better antihypertensive effect of P-adrenoceptor blockers is found in patients having high PRA and most are not efficacious in patients having low PRA or in elderly patients. P-Adrenoceptor blockers usually lower arterial blood pressure about 10 mm Hg (1.3 kPa). Side effects include lethargy, dyspnea, nausea, dizziness, headache, impotency, cold hands and feet, vivid dreams and nightmares, bronchospasm, bradycardia, and sleep disturbances. 

Calcium channel blockers reduce arterial blood pressure by decreasing calcium influx, resulting in a decrease in intracellular calcium (236,237). The arterial smooth muscle tone decreases, thereby decreasing total peripheral resistance. The increase in vascular resistance in hypertension is found to depend much on calcium influx. Calcium channel blockers reduce blood pressure at rest and during exercise. They decrease the transmembranous calcium influx or entry that lead to a net decrease of intracellular calcium and therefore the vascular tone falls, as does blood pressure. 

Methyldopa. Methyldopa reduces arterial blood pressure by decreasing adrenergic outflow and decreasing total peripheral resistance and heart rate having no change in cardiac output. Blood flow to the kidneys is not changed and that to the heart is increased. It causes regression of myocardial hypertrophy. 

Methyldopa, through its metaboHte, CX-methyInorepinephrine formed in the brain, acts on the postsynaptic tt2-adrenoceptor in the central nervous system. It reduces the adrenergic outflow to the cardiovascular system, thereby decreasing arterial blood pressure. If the conversion of methyldopa to CX-methyl norepinephrine in the brain is prevented by a dopamine -hydroxylase inhibitor capable of penetrating into the brain, it loses its antihypertensive effects. 

The median lethal dose of lunacrine hydrochloride is 78-7 3-8 mgm. per kilo given intravenously in mice. Oral doses of 1 gramme of lunamarine are not fatal. The m.l.d. of lunacridine by mouth is 1,097 167 mgra. per kilo. Limamarine stimulates isolated rabbit intestine and uterus, but lunacrine and lunacridine inhibit peristaltic movement of the isolated intestine. All three alkaloids reduce arterial blood pressure in cats. ... 

Baroreceptor. Specialized pressure-sensitive tissue located in carotid arteries. Nerve impulses proportional to arterial blood pressure are conducted from this tissue to the brain which in turn exerts control over the blood pressure. 

DHPs are potent arterial vasodilators. They act on resistance vessels and therefore reduce peripheral vascular resistance, lower arterial blood pressure, and antagonize vasospasms in coronary or peripheral arteries. By reducing afterload, DHPs also reduce cardiac oxygen demand. Together with their vascular spasmolytic effect, this explains most of the beneficial actions of DHPs in angina pectoris. Most DHPs are only licensed for the therapy of hypertension, some of them also for the treatment of angina pectoris and vasospastic (Prinzmetal) angina. 

To characterize the responses to PbTx-2, five dose rates (0, 12.5, 25, 50, and 100 ig/kg/hr in 2 ml saline) were infused into the jugular catheters of rats (four per group). Heart rates, systolic and diastolic arterial blood pressures, pulse pressures, respiratory rates, core and peripheral body temperatures, lead VI0 ECCjs, and arterial blood gases were monitored. Clinical signs and behaviors were recorded by video camera. After infusion, animals were monitored for 6 hr, by which time most had either died or recovered to near baseline physiological levels. 

After initial experiments demonstrating that the antiserum was capable of completely inhibiting the binding of [ H]PbTx-3 to its receptor site in rat brain membranes (Figure 9), we began studies designed to evaluate potential of the antiserum for prophylaxis and treatment of brevetoxin intoxication (34). The tethered rat model was used, and surgical implantations were identical to those described above. Heart rate, core and peripheral body temperatures, lead VIO ECG, and arterial blood pressure were monitored continuously. Respiratory rate was recorded each 5 min for the first 3 hr, then each 15 min until 6 hr. 

Practitioners must have a good understanding of cardiovascular physiology to diagnose, treat, and monitor circulatory problems in critically ill patients. Eugene Braunwald, a renowned cardiologist, described the interrelationships between the major hemodynamic variables (Fig. 10-1).1 These variables include arterial blood pressure, cardiac output (CO), systemic vascular resistance (SVR), heart rate (HR), stroke volume (SV), left ventricular size, afterload, myocardial contractility, and preload. While an oversim-... 

Has the goal arterial blood pressure been achieved If not, give additional fluid therapy hourly blending crystalloids and isooncotic colloids based on inadequate blood pressure response. 

ABP Arterial blood pressure disease antibiotic removal device aphakic retinal... 

Mean arterial blood pressure A calculated measure of arterial blood pressure mean arterial blood pressure = (2 x diastolic blood pressure + systolic blood pressure)/3. 

Systemic vascular resistance The portion of resistance to blood flow leaving the heart that is determined by vascular tone (constriction or relaxation). Systemic vascular resistance = mean arterial blood pressure/cardiac output. 

Other factors regulating ADH secretion include blood volume and blood pressure. A decrease in blood volume of 10% or more causes an increase in ADH secretion sufficient to cause vasoconstriction as well as antidiuresis. A decrease in mean arterial blood pressure of 5% or more also causes an increase in ADH secretion. The resulting water conservation and vasoconstriction help increase... 

The macula densa, which is involved in tubuloglomerular feedback, is also a factor in the regulation of renin secretion. In fact, this mechanism involving the macula densa is thought to be important in the maintenance of arterial blood pressure under conditions of decreased blood volume. For example, a decrease in blood volume leads to a decrease in RBF, GFR, and filtrate flow through the distal tubule. The resulting decrease in the delivery of NaCl to the macula densa stimulates the secretion of renin. Increased formation of angiotensin II serves to increase MAP and maintain blood flow to the tissues. 

Rokosh, D. G. and Simpson, P. C. Knockout of the alpha lA/C-adrenergic receptor subtype the alpha 1A/C is expressed in resistance arteries and is required to maintain arterial blood pressure. Proc. Natl Acad. Sci. U.S.A. 99 9474-9479, 2002. 

Tanoue, A., Nasa, Y., Koshimizu, T. etal. The alpha(lD)-adrenergic receptor directly regulates arterial blood pressure via vasoconstriction. /. Clin. Invest. 109 765-775, 2002. 

Slowing of fetal heart rate, disruption of respiratory movements, significant but inconsistent changes in arterial blood pressure... 

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