Blood pressure, causes

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

Reduction in blood pressure caused by treprostinil may be exacerbated by drugs that by themselves alter blood pressure, such as diuretics, antihypertensive agents, or vasodilators. Because treprostinil inhibits platelet aggregation, there is also a potential for increased risk of bleeding, particularly among patients maintained on anticoagulants. 

Conflicting results have been reported in regard to the involvement of beta receptors in the mechanism of the Inotropic effect of 2-PAM. It was concluded that the direct stimulation of the myocardium by 2-PAM that could be blocked by dichloroisoproterenol (DCI) was responsible for the increase in blood pressure.3 A recent report, however, has indicated that the Increase in blood pressure caused in the dog by 2-PAM was not blocked by propranolol.1 ... 

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

As indicated in Fig. 25-18, free adenine released from catabolism of nucleic acids can be deaminated hydrolytically to hypoxanthine, and guanine can be deaminated to xanthine.328 The molybdenum-containing xanthine oxidase (Chapter 16) oxidizes hypoxanthine to xanthine and the latter on to uric acid. Some Clostridia convert purine or hypoxanthine to xanthine by the action of a selenium-containing purine hydroxylase.3283 Another reaction of xanthine occurring in some plants is conversion to the trimethylated derivative caffeine. 328b One of the physiological effects of caffeine in animals is inhibition of pyrimidine synthesis.329 However, the effect most sought by coffee drinkers may be an increase in blood pressure caused by occupancy of adenosine receptors by caffeine.330... 

Reflex arcs Most of the afferent impulses are translated into reflex responses without involving consciousness. For example, a fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the heart, vena cava, aortic arch, and carotid sinuses) to send fewer impulses to cardiovascular centers in the brain. This prompts a reflex response of increased sympathetic output to the heart and vasculature, and decreased parasympathetic output to the heart, which results in a compensatory rise in blood pressure and tachycardia (see Figure 3.5). 

Adverse effects Verapamil and diltiazem have negative inotropic properties and therefore may be contraindicated in patients with preexisting depressed cardiac function. Both drugs can also cause a decrease in blood pressure caused by peripheral vasodilation. 

Russell RWR. How does blood-pressure cause stroke Lancet 1975 ii 1283-5. 

Accelerated phase hypertension was previously called malignant hypertension because the lack of treatment heralded death within a year of diagnosis. It is characterised pathologically by fibrinoid necrosis of the small arteries. An important consequence is the loss of autoregulation of the cerebral and renal circulation, so that any reduction in blood pressure causes a proportional fall in perfusion of... 

We are interested in high blood pressure (hypertension) because of our interest in cardiovascular disease, a leading cause of morbidity and mortality. High blood pressure is a meaningful and useful cardiovascular surrogate endpoint because it is well established that chronic high blood pressure causes cardiovascular and cerebrovascular events. 

It has been established that hypothalamic, and possibly other areas of the brain, also contain both types of adrenoceptors on neurons. The effect on blood pressure caused by receptor stimulation is opposite to that in the peripheral smooth musculature. That is, a-stimulation of these brain receptors results in a decrease in stimulation due to the inhibitory effect of sympathetic outflow (see Chapter 9). 

Circulation Atropine, alone, has httle effect on blood pressure, an expected result since most vessels lack chohnergic innervation. However, in clinical doses, atropine completely counteracts the peripheral vasodilation and sharp fall in blood pressure caused by chohne esters. Atropine in toxic, and occasionally therapeutic, doses can dilate cutaneous blood vessels, especially those in the blush area (atropine flush). 

Leikola, E. and E. Rautavaara Der Anteil des Kohlenmonoxid an der durch des Tabakrauchen verursa-chten Blutsdrucksteigerung [The importance of carbon monoxide in the increase in blood pressure caused by tobacco smoking] Acta Soc. Med. Finn. Duodecrm. 16 (1934) 3-25. 

Figure 11-2-4 summarizes the effects of ganglionic blockers on drugs that modify blood pressure, causing a reflex change in heart rate, and on drugs that act directly at the SA node to change the heart rate. 

A) Decreased blood pressure caused by hexamethonium Increased blood pressure caused by nicotine Increased skeletal muscle strength caused by neostigmine Tachycardia caused by exercise Tachycardia caused by infusion of acetylcholine Which of the following best describes the mechanism of action of scopolamine ... 

Patients with pheochromocytoma may have this tumor for several months or even years before symptoms or signs lead to a diagnosis. Predict the probable eompensatory responses to a chronic increase in blood pressure caused by a tumor releasing laige amounts of norepinephrine. Skill Keeper Answer appears at the end of the chapter. 

C. Slow intravenous infusion (< 0.3 mg/min) may result in transient increased blood pressure caused by stimulation of beta-adrenergic receptors. 

Precautions Can raise blood pressure, cause heart palpitations, stroke, memory loss, nerve damage, and psychosis. Some states and the FDA plan to restrict its use. 

The manufacturer notes that atomoxetine 60 mg twice daily for 5 days potentiated the increase in heart rate and blood pressure caused by an infusion of salbutamol 600 micrograms over 2 hours. Because of this, they recommend caution when atomoxetine is used in patients receiving intravenous or oral salbutamol or other beta2 agonists (for a list, see Table 33. r, (p.ll59)). The UK manufacturer also extends this precaution to high-dose nebulised salbutamol. ... 

Experimental studies in healthy subjects, on the way xanthine drugs possibly interact with adenosine, have shown that caffeine and theophylline (but not enprofylline) reduced the increased heart rate and the changes in blood pressure caused by infusions of adenosine, and attenuated adenosine-induced vasodilatation. Theophylline also attenuated adenosine-induced respiratory effects and chest pain. Similarly, an adenosine infusion antagonised the haemodynamic effects of a single dose of theophylline in healthy subjects, but did not reduce the metabolic effects (reductions in plasma potassium and magnesium). ... 

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