Final answer:
Nitric oxide primarily activates guanylate cyclase, which leads to the production of cGMP, causing vasodilation and smooth muscle relaxation. It does not activate adrenergic receptors, increase intracellular calcium, or enhance sodium reabsorption.
Step-by-step explanation:
The mechanism and physiologic effects of nitric oxide (NO) are substantial, particularly regarding vasodilation and cardiovascular health. Among the options provided, NO activates guanylate cyclase, an intracellular enzyme, leading to the production of cyclic guanosine monophosphate (cGMP). cGMP acts as a second messenger causing smooth muscle relaxation, which is conducive to vasodilation. Vasodilation increases blood flow and as such is a critical mechanism supported by NO in the physiological context. Contrary to adrenergic receptors, which are typically associated with responses to adrenaline and noradrenaline, NO does not directly activate adrenergic receptors.
NO does not increase intracellular calcium; instead, through cGMP, it may lead to a reduction in calcium concentrations causing relaxation rather than contraction of smooth muscles. This is opposite to the action of alpha-1 adrenergic receptors, which, upon activation, cause vasoconstriction and an increase in intracellular calcium. Lastly, NO does not enhance sodium reabsorption; in fact, it decreases blood pressure and does not emphasize reabsorption in the kidneys.