Vessels capacitance

Nasal vasculature may offer some insight into this question, though research to date has been equivocal. Nasal turbinate vessels can be classified as either capacitance vessels or resistive vessels. Capacitance vessels appear to vasodilate in response to infection while resistance vessels appear to respond to cold stimuli by vasoconstriction. Buccal vascular structures also respond to thermal stimuli but appear to respond principally to cutaneous stimuli. How pharyngeal and tracheobronchial submucosal vessels react to thermal stimuli is not known, though cold-induced asthma is believed to result from broncho-spasms caused by susceptible bronchial smooth muscle responding to exposure to cold dry air.- This asthmatic response suggests an inadequate vascular response to surface cooling. 

Capacitance vessels Larger venules and veins forming a large-volume, low-... 

Decongestants such as OTC pseudoephedrine are sympathomimetic agents that constrict capacitance vessels in the nasal turbinates.17 Decongestants effectively reduce nasal congestion and to some extent rhinorrhea associated with AR.8,12 The recommended dose of pseudoephedrine is 30 to 60 mg every 4 to 6 hours for a maximum daily dose of 240 mg.15 Systemic adverse effects such as irritability, dizziness, headache, tremor, tachycardia, and insomnia can occur. Additionally, use is associated with increased blood pressure and intraocular pressure and urinary obstruction.8,12... 

The answer is b. (tlardman, p 229. Katzung, p 168.) Terazosin blocks a receptors in arterioles and venules It is 0 -selective. Perhaps this selectivity permits NE to exert unopposed negative feedback on its own release because of little or no effect on presynaptic a.2 receptors. Alpha blockers reduce arterial pressure in both resistance and capacitance vessels andT thereforet are quite effective in reducing blood pressure when a patient is in the upright position... 

The inhibition of sympathetic tone to the venous system (capacitance vessels) results in increased pooling of blood in the venous vascular bed with consequent decreased venous return to the heart and decreased cardiac output. This phenomenon is more pronounced in upright positions because of the effect of gravity. The hemodynamic effects of ganglionic blockers include decreases in cardiac output, renal blood flow, cerebral blood flow and orthostatic hypotension(20,21). 

In heart failure, cardiac output rises again because ventricular afterload diminishes due to a fall in peripheral resistance. Venous congestion abates as a result of (1) increased cardiac output and (2) reduction in venous return (decreased aldosterone secretion, decreased tonus of venous capacitance vessels). 

O -Adrenoceptor antagonists (o -blockers) are competitive inhibitors at the level of Q -adrenoceptors. These receptors are found in many organs and tissues, but their predominant functional importance is to mediate the vasoconstrictor effects of endogenous catecholamines (noradrenaline, adrenaline) released from the sympathetic nerve endings. Conversely, Q -adrenoceptor antagonism by means of an a-blocker will inhibit this constrictor activity and hence cause vasodilatation. This vasodilator effect occurs in both resistance vessels (arterioles) and capacitance vessels (veins), since a-adrenoceptors are present in both types of vascular structures. Accordingly, both cardiac afterload and preload will be lowered, in particular when elevated. 

Physiologically, in both normal and hypertensive individuals, blood pressure is maintained by moment-to-moment regulation of cardiac output and peripheral vascular resistance, exerted at three anatomic sites (Figure 11-1) arterioles, postcapillary venules (capacitance vessels), and heart. A fourth anatomic control site, the kidney, contributes to maintenance of blood pressure by regulating the volume of intravascular fluid. Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure. Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 (see Chapter 17) constricts and nitric oxide (see Chapter 19) dilates blood vessels. 

Blood pressure lowering by clonidine results from reduction of cardiac output due to decreased heart rate and relaxation of capacitance vessels, with a reduction in peripheral vascular resistance. 

The hypotensive action of guanethidine early in the course of therapy is associated with reduced cardiac output, due to bradycardia and relaxation of capacitance vessels. With long-term therapy, peripheral vascular resistance decreases. Compensatory sodium and water retention may be marked... 

Alpha blockers reduce arterial pressure by dilating both resistance and capacitance vessels. As expected, blood pressure is reduced more in the upright than in the supine position. Retention of salt and water occurs when these drugs are administered without a diuretic. The drugs are more effective when used in combination with other agents, such as a 13-blocker and a diuretic, than when used alone. 

This drug causes dilation of resistance vessels (arterioles) but not of capacitance vessels (venules). Minoxidil [mi NOX i dill] is administered orally for treatment of severe to malignant hypertension that is... 

Sinus tachycardia (due to vagal blockade) is a common feature but abnormalities of cardiac conduction accompany moderate to severe intoxication and may proceed to dangerous tachy- or bradyarrhythmias. Hypoterrsion may result from a combination of cardiac arrhythmia, reduced myocardial contractility and dilatation of venous capacitance vessels. 

Dilatation of venous capacitance vessels reduced venous return to the heart (preload) leads to reduced cardiac output, especially in the upright position... 

Midodrine is a prodrug, whose active metabolite is relatively selective for vascular postjunctional alphai-adrenoceptors and therefore increases peripheral resistance by arteriolar constriction, with some veno-constriction in capacitance vessels (1). It has minimal activity in the central nervous system, since it does not cross the blood-brain barrier. It can be given orally and has a systemic availabihty of over 90% by this route. The half-life of the active deglycinated metabolite is relatively short (2-3 hours). The dosage range is 2.5-10 mg tds, and is usually toward the upper end of this range. 

---