Vascular effects, high-dose lead

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

The emphasis in this question is on the word acute. An acute dose of ethanol relaxes both vascular and uterine smooth muscle. Vasodilation occurs and at high doses may lead to hypothermia. Blood pressure is not raised acutely, though chronic use of alcohol is a risk factor for hypertension. The effect of ethanol on the uterus is to prolong labor. The other effects listed are associated with chronic ethanol use. The answer is (D). 

In recent years, interest in the clinical problems related to low-level lead exposure has directed experimental attention away from high-dose systems with vascular encephalopathic changes to others where lower doses of lead are given in an attempt to identify less dramatic neurotoxic effects. Table 4 lists a number of experimental systems abstracted from the literature of the past 16 years. In these, rats have been subjected to lead exposure via every conceivable route of administration, and a bewildering number of doses. 

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. 

Recently, Tsubosaka et al. (2010a) reported that halichlorine was also revealed to inhibit L-type Ca2+ channels, which leads to inhibit smooth muscle contraction. In their report, the direct effect of halichlorine on vascular contractility was investigated. Then, halichlorine was found to inhibit both high concentration of K+- and phenylephrine-induced contractions in rat aorta dose dependently. The effect of halichlorine on high K+-induced contraction was shown to be stronger than that on phenylephrine-induced contraction. Because known L-type Ca2+ channel blockers, verapamil and nifedipine, were observed to show the similar effect by them, it was suggested that halichlorine selectively inhibits L-type Ca2+ channels. Then, the effect of halichlorine on intracellular Ca2+ concentration in vascular smooth muscle tissue was examined using a fluorescent Ca2+ indicator, Fura-2. 

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... 

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