Heart and vasculature

AM is widely distributed in the body. The highest concentrations are found in the adrenal glands, hypothalamus, and anterior pituitary, but high levels are also present in the kidneys, lungs, cardiovascular system, and gastrointestinal tract. AM in plasma apparently originates in the heart and vasculature. 

Angiotensin II receptor blockers Eprosartan (Teveten] Losartan (Cozaar] Valsartan (Diovan] Reduce angiotensin ll-induced peripheral vascular resistance and cardiovascular hypertrophy/remodeling by blocking angiotensin II receptors on the heart and vasculature... 

In addition to its normal role in controlling fluid and electrolyte balance, aldosterone can have detrimental effects on the heart and vasculature. Excess or prolonged aldosterone production can cause hypertrophy and fibrosis of cardiac and vascular tissues and lead to detrimental changes in these tissues.30,78 Moreover, it is now apparent that aldosterone can be produced locally within certain tissues including the heart and vascular endothelium.78,83 That is, these tissues may produce their own supply of aldosterone as well as receive circulating levels of aldosterone from the... 

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). 

In several papers the Kunos group has reported observations that may represent a starting point for novel medicinal chemistry research in this area [167, 168], Anandamide (i.v. bolus 4 mg/kg) caused a triphasic blood pressure response, brief hypotension, followed by a transient pressor and then a prolonged depressor phase. The hypotensive effect was not initiated in the CNS, but was due to a presynaptic action that inhibited norepinephrine release from sympathetic nerve terminals in the periphery (heart and vasculature). The inhibitory effect (but not the pressor effect) was antagonized by SR141716A, indicating that this peripheral action was mediated by CB receptors. 

The sympathetic adrenergic nervous system plays a major role in the regulation of arterial pressure. Activation of these nerves to the heart increases the heart rate (positive chronotropy), contractility (positive inotropy), and velocity of electrical impulse conduction (positive dromotropy). Within the medulla are located preganglionic sympathetic excitatory neurons, which travel from the spinal cord to the ganglia. They have significant basal activity, which generates a level of sympathetic tone to the heart and vasculature even under basal conditions. The sympathetic ... 

Once the heart and vasculature are linked, neural and hormonal controls need to be added. These include the baroreflex, the chemoreflex, the renin-angiotensin reflex, capillary fluid shift, autoregulation, stress relaxation, and renal-body-fluid balance (water intake and urine output). 

Heart and Vasculature 4-NP, and to a greater extent 4-OP and 17P-estradiol, had the capacity to increase coronary perfusion pressure when administered at 100 nanomolar (nM) to perfused rat hearts (Ruehlmann et al. 1998). Investigators further demonstrated that 4-OP and estradiol can act on vasculature by inhibition of L-type Ca " channels in smooth muscle cells, suggesting an estrogen-related effect of APs on cardiac tissue. 

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