Resistance vessels

Nifedipine (Table 3) is a potent vasodilator that selectively dilates resistance vessels and has fewer effects on venous vessels. It does not cause reflex tachycardia during chronic therapy. Nifedipine is one of the first-line choices for black or elderly patients and patients having concomitant angina pectoris, diabetes, or peripheral vascular diseases. Nifedipine, sublingually, is also suitable for the treatment of hypertensive emergencies. Nifedipine does not impair sexual function or worsen blood Hpid profile. The side effects are flushing, headache, and dizziness. 

Containment (Explosion-Pressure-Resistant Design for Maximum Explosion Overpressure) An explosion-resistant construction is understood to mean the possibihty of designing vessels and equipment for the full maximum explosion ove (pressure, which is generally of the order P = 9 bar. The explosion-resistant vessel can then be designed as explosion pressure resistant or explosion pressure shock resistant. This protective measure is generally employed when small vessel volumes need to be protected, such as small filter units, fluidized-bed dryers, cyclones, rotaiy valves, or mill housings. 

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. 

Resistance vessels Microcirculatory blood vessels (arterioles, pre-capillary... 

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. 

Figure 15.1 The circulatory system. Arteries carry blood away from the heart. The smallest arterial vessels, the arterioles, are composed mainly of smooth muscle and are the major resistance vessels in the circuit. The capillaries are the site of exchange between blood and tissues. Veins carry blood back toward the heart. The small veins are the major compliance vessels in the circuit and, under resting conditions, contain 64% of the blood volume.

Therefore, depending upon the degree of constriction of the vascular smooth muscle, these vessels may alter their diameter, and consequently their blood flow, across a very wide range. For this reason, the arterioles are the major resistance vessels in the circulatory system. In fact, the primary function of arterioles is to regulate the distribution of the cardiac output and to determine which tissues receive more blood and which receive less, depending upon the tissue s and the body s needs. 

As mentioned previously, the arterioles are the major resistance vessels in the circulatory system. Because the walls of these vessels contain primarily smooth muscle, they are capable of significant changes in their radius. Therefore, regulation of blood flow to the tissues is carried out by the arterioles. 

Total peripheral resistance (TPR) is the resistance to blood flow offered by all systemic vessels taken together, especially by the arterioles, which are the primary resistance vessels. Therefore, MAP is regulated by cardiac activity and vascular smooth muscle tone. Any change in CO or TPR causes a change in MAP. The major factors that affect CO, TPR, and therefore MAP, are summarized in Figure 15.3, as well as in Table 15.1. These factors may be organized into several categories and will be discussed as such ... 

The caliber of the resistance vessels delivering blood to the myocardium and MVo2 are the prime determinants in the occurrence of ischemia. 

Containment Containment is understood to mean the possibility of designing vessels and equipment for the full maximum explosion overpressure, which is generally from = 7 to 10 bar. The explosion-resistant vessel can then be designed as explosion-pressure-resistant or... 

Most average homes contain a microwave oven. Researchers have taken that same technology and applied it to sample extraction. Using microwave technology with acidic solutions has become a commonplace replacement for traditional acid digests. The sample is placed in a closed, chemical-resistant vessel and heated in a microwave. This process is much faster than hot-plate techniques and has become widely accepted by such agencies as the US EPA. 

Jiang X, Wang Y, Hand AR, Gillies C, Cone RE, Kirk J, O Rourke J Storage and release of tissue plasminogen activator by sympathetic axons in resistance vessel walls. Microvasc Res 2002 64 438-447. 

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. 

Minoxidil is a potent vasodilator predominantly with respect to resistance vessels. Vasodilatation is brought about, at least in part, by the opening of potassium channels, thus causing hyperpolarisation... 

Dihydropyridines are predominantly vasodilator dmgs at the level of resistance vessels (precapillary arterioles) and to a certain degree also in the... 

Conversely, the suppression of the biosynthesis of Ang II via ACE-inhibition will lead to vasodilatation, reduced release of aldosterone, blunting of sympathetic stimuli, and impairment of myocardial and vascular hypertrophy. The antihypertensive effect of the ACE-inhibitors is readily explained on the basis of vasodilatation, which occurs predominantly in the resistance vessels (arterioles) and, to a lesser extent, also in the venous system. Vasodilatation by... 

The glomerulus is situated between two sets of resistance vessels, the afferent and efferent arterioles, thus preventing transmission of this pressure to the glomerulus. This compensatory mechanism may be one explanation for the relatively low incidence of hypertensive nephrosclerosis (1.5-4%) among patients with mile to moderate hypertension. In the intrarenal vasculature, angiotensin receptors are found in greater density in the efferent... 

Direct vasodilators reduce pressure by dilating resistance vessels (arteries) by vascular smooth muscle relaxation (e.g., Ca + channel blockers such as verapamil (4.133) or nifedipine (5.151) vasodilators such as dihydralazine (5.152))... 

It is an piperazinyl quinazoline effective in the management of hypertension. It is highly selective for receptors. It also reduces the venous return and cardiac output. It is used in essential hypertension, benign prostatic hypertrophy and in Raynaud s syndrome. Prazosin lowers blood pressure in human beings by relaxing both veins and resistance vessels but it dilates arterioles more than veins. 

It is a coronary dilator and claimed to dilate coronary resistance vessels. It probably... 

Intravenous administration of dopamine promotes vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels, via activation of Di receptors. Activation of the Di receptors in the renal vasculature may also induce natriuresis. The renal effects of dopamine have been used clinically to improve perfusion to the kidney in situations of oliguria (abnormally low urinary output). The activation of presynaptic D2 receptors suppresses norepinephrine release, but it is unclear if this contributes to cardiovascular effects of dopamine. In addition, dopamine activates Bj receptors in the heart. At low doses, peripheral resistance may decrease. At higher rates of infusion, dopamine activates vascular a. receptors, leading to vasoconstriction, including in the renal vascular bed. Consequently, high rates of infusion of dopamine may mimic the actions of epinephrine. 

Direct vasodilators, which reduce pressure by relaxing vascular smooth muscle, thus dilating resistance vessels and—to varying degrees—increasing capacitance as well. 

In animals, AM dilates resistance vessels in the kidney, brain, lung, hind limbs, and mesentery, resulting in a marked, long-lasting hypotension. The hypotension in turn causes reflex increases in heart rate and cardiac output. These responses also occur during intravenous infusion of the peptide in healthy human subjects. AM also acts on the kidneys to increase sodium excretion, and it exerts several endocrine effects including inhibition of aldosterone and insulin secretion. It acts on the central nervous system to increase sympathetic outflow. 

Sodium cells20-23 operate at fairly high temperatures (300-400 °C) and require an inert atmosphere (argon) in a sealed, corrosion-resistant vessel (e.g., Cr-coated steel). Furthermore, leakage of liquid Na could obviously have dire consequences. Nevertheless, sodium-sulfur cells have received serious consideration as rechargeable batteries ... 

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