Arteries resistance

Elevated peripheral arterial resistance is a hallmark of primary hypertension. The increase in peripheral resistance typically observed may be due to a reduction in the arterial lumen size as a result of vascular remodeling. This remodeling, or change in vascular tone, may be modulated by various endothelium-derived vasoactive substances, growth factors, and cytokines. This increase in arterial stiffness or reduced compliance results in the observed increase in systolic blood pressure.9... 

Sympathetic and parasympathetic nerves innervate the penis. In the flaccid state, OC2-adrenergic receptors mediate tonic contraction of the arterial and corporal smooth muscles. This maintains high penile arterial resistance and a balance exists between blood flow into and out of the corpora. With sexual stimulation, nerve impulses from the brain travel down the spinal cord to the thoracolumbar ganglia.3 A decrease in sympathetic tone and an increase in parasympathetic activity then occurs, causing a net increase in blood flow into the erectile tissue. Erections may also occur as a result of a sacral nerve reflex arc while patients are sleeping (nocturnal erections). 

Ramipril (Altace) Angiotensin converting enzyme (ACE) inhibitor Inhibits ACE, decreases peripheral arterial resistance... 

Mechanism of Action An ACE inhibitor that decreases the rate of conversion of angiotensin I to angiotensin 11, a potent vasoconstrictor Reduces peripheral arterial resistance. Therapeutic Effect Lowers BP. 

Mechanism of Action AnACE inhibitor that suppresses the renin-angiotensin-aldos-terone system and prevents conversion of angiotensin I to angiotensin 11, a potent vasoconstrictor may also inhibit angiotensin II at local vascular and renal sites. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance, pulmonary capillary wedge pressure improves cardiac output and exercise tolerance. Pharmacokinetics ... 

Mechanism of Action An ACE inhibitor that suppresses the renin-angiotensin-aldosterone system. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance and BP. 

Alpha receptors are widely expressed in vascular beds, and their activation leads to arterial and venoconstriction. Their direct effect on cardiac function is of relatively less importance. A relatively pure agonist such as phenylephrine increases peripheral arterial resistance and decreases venous capacitance. The enhanced arterial resistance usually leads to a dose-dependent rise in blood pressure (Figure 9-... 

Chapter 12 contains additional discussion of vasodilators. All the vasodilators that are useful in hypertension relax smooth muscle of arterioles, thereby decreasing systemic vascular resistance. Sodium nitroprusside and the nitrates also relax veins. Decreased arterial resistance and decreased mean arterial blood pressure elicit compensatory responses, mediated by baroreceptors and the sympathetic nervous system (Figure 11-4), as well as renin, angiotensin, and aldosterone. Because sympathetic reflexes are intact, vasodilator therapy does not cause orthostatic hypotension or sexual dysfunction. 

Vascular smooth muscle tone is regulated by adrenoceptors consequently, catecholamines are important in controlling peripheral vascular resistance and venous capacitance. Alpha receptors increase arterial resistance, whereas 2 receptors promote smooth muscle relaxation. There are major differences in receptor types in the various vascular beds (Table 9-4). The skin vessels have predominantly receptors and constrict in the presence of epinephrine and norepinephrine, as do the splanchnic vessels. Vessels in skeletal muscle may constrict or dilate depending on whether ffor 13 receptors are activated. Consequently, the overall effects of a sympathomimetic drug on blood vessels depend on the relative activities of that drug at and 8receptors and the anatomic sites of the vessels affected. In addition, Di receptors promote vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels. Activation of the Di receptors in the renal vasculature may play a major role in the natriuresis induced by pharmacologic administration of dopamine. 

Mental stress can trigger a lack of blood flow to the heart, thus heightening the risk of death in people who already have clogged arteries. Such mental stress increases oxygen demand because blood pressure and heart rate go up. At the same time, stiffened arteries resist the greater blood flow and coronary arteries in the heart constrict, further decreasing the blood supply. 

Carrier M,Tronc F, Stewart D, Pelletier FC. Dose-dependent effect of cyclosporin on renal arterial resistance in dogs. Am J Physiol 1991 261 H1791-H1796. 

Several factors, such as preload, afterload, heart rate and contractility, determine normal cardiovascular function. Contractility is affected both by preload and afterload, as well as the inotropic state of the ventricular myocardium. Preload is the diastolic load placed upon the ventricle by the venous return of blood and affects contractility as described by Starling s law of the heart, where increased diastolic volume leads to a greater force of contraction. Preload is affected by the venous tone and by the circulating blood volume. Afterload opposes contraction throughout systole and is determined by the arterial resistance and by the circulating blood volume. 

Nifedipine given intravenously increases forearm blood flow with little effect on venous pooling this indicates a selective dilation of arterial resistance vessels. The decrease in arterial blood pressure elicits sympathetic reflexes, with resulting tachycardia and positive inotropy. Nifedipine also has direct negative inotropic effects in vitro. However, nifedipine relaxes vascular smooth muscle at significantly lower concentrations than those required for prominent direct effects on the heart. Thus, arteriolar resistance and blood pressure are lowered, contractility and segmental ventricular function are improved, and heart rate and cardiac output are increased modestly. After oral administration of nifedipine, arterial dilation increases peripheral blood flow venous tone does not change. 

DA also causes the release of NE from nerve terminals, which contributes to its effects on the heart. DA usually increases systolic blood pressure and pulse pressure and either has no effect on diastolic blood pressure or increases it slightly. Total peripheral resistance usually is unchanged when low or intermediate doses of DA are given, probably because of reduced regional arterial resistance in some vascular beds (e.g., mesenteric and renal) with minor increases in others. At high concentrations, DA activates vascular receptors, leading to more... 

It is a potent synthetic opiate analgesic that gets completely absorbed from the G1 tract after oral administration and, importantly, it undergoes almost 80% first-pass metabolism. It has been duly established that this drug enhances arterial resistance and the work of the heart (an action very much akin to petazocine ) consequently, it is usually contra indicated in such patients who have a history of acute myocardial infarction. 

Reduces peripheral arterial resistance in hypertensive patient, possibly by inhibiting angiotensin converting enzyme (ACE). 

Based on the above considerations, it is conceivable that some hemodynamic adjustments (i.e., cardiac output and vascular changes) may also follow primary modifications in metabolic demand. In this context, the decrease in cardiac output and increase in peripheral arterial resistance and diastolic BP in the hypothyroid state may be interpreted as the final result of an adaptive response to the reduction in tissue metabolic activities. 

A low thyroid function can influence many of the neuro-humoral systems involved in vascular tone and plasma volume regulation. It has long been known that chronic hypothyroid patients show an increase in peripheral arterial resistance. This is principally due to the lack of direct T3-dependent vasorelaxation and to an increase in arterial wall thickness (Cappola and Ladenson, 2003 Rawat and Satyal, 2004), but enhanced sympathetic activity may also contribute significantly to peripheral vasoconstriction, probably as a powerful compensatory mechanism for the decreased cardiac contractility and intravascular volume which follows TH deprivation. The enhanced sympathetic efflux may eventually overcome a downregulation of post-synaptic vasoconstrictor a-adrenoreceptors, which is described in hypothyroid states, at variance with what is observed in normal physiology, where a positive relationship does exist between TH and the number and activities of noradrenergic receptors (Gomberg-Maitland and Frishman, 1998). 

B. Low-dose infusion is most effective tor hypotension caused by venodiiation or reduced cardiac contractiiity high-dose dopamine is indicated for shock resulting from decreased peripheral arterial resistance. 

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