Q#4: Outline how this drug works to lower BP in the human body
The peripheral acting adrenergic inhibitors or antagonists mainly reduce the overall small arteries blood flow by inhibiting the release of epinephrine and nor epinephrine. Some of the key drugs in this class include reserpine. Increased sympathoadrenal activity helps in maintaining elevated blood pressure in patients with hypertension. Altering the adregenic receptor can contribute to increased sympathoadrenal activity. The adrenergic receptors in hypertensive patients are mainly regulated by the presence of catecholamines. Peripheral adrenergic Inhibitors depletes NE from the postganglionic sympathetic neurons thereby decreasing activation of the adrenergic receptors. The adrenergic inhibitors produces the effects similar to these produced by the beta-adrenergic blockade and alpha-adrenergic blockage (Michel, Brodde, &, Insel, 1990, pp. 107-120)..
Mechanism of NE depletion
NE depletion occurs in two main ways. The drug first causes the displacement of the NE stored within the nerve terminal by acting on the vesicle contained therein. The displacement exposes the entire transmitter allowing monoamine oxidase to destroy them (Barcelos, et al, 2010, pp. 143–149).
The other way that the NE is depleted is by suppressing the synthesis of NE. the inhibitors block the raw uptake of dopamine into the presymaptic vesicle containing the enzymes responsible for converting the dopamine into NE. This means that the release of NE is inhibited. Finally, the inhibition process is also affected by the depletion of the serotonin and catecholamine’s from CNS Neurons
The drug taken only acts by
Reserpine irreversibly blocks the vesicular monoamine transporter (VMAT). This normally transports free intracellularnorepinephrine, serotonin, and dopamine in the presynaptic nerve terminal into presynaptic vesicles for subsequent release into the synaptic cleft (“exocytosis”). Unprotected neurotransmitters are metabolized by MAO (as well as by COMT) in the cytoplasm and consequently never excite the post-synaptic cell (Michel, Brodde, &, Insel, 1990, pp. 107-120).
Q#6. Pretend that your grandparent or someone else you know was just prescribed the type of drug that you wrote about for Question #4. Now write as if you are explaining to your grandparent how the drug works to control blood pressure
The drug taken only acts by decreasing the systolic blood pressure more than the diastolic blood pressure. I it is also important to note that the mechanisms of drug action include producing a selective block of efferent, peripheral sympathetic pathway. The drug replaces and depletes the norepinephrine stores from the adrenergic nerve endings thereby preventing the adrenergic nerve endings from producing the norepinephrione from the adrenal medulla. This also depletes the norepinephrine stored in the GI tract. These drugs also vasodilators as the n open the blood vessels. Their point of action is on the arterial wall muscles thereby stopping the muscle from being so tight and narrow and allows blood to pass through the walls (Lindmar, löffelholz, &, Muscholl, 1968, pp. 280–294).
When blood flows through the walls to the artery, the chances of blood pressure increasing is reduced, as the heart does not gave to pump so hard to pass the blood through the walls of the artery. When there are arterial resistance the drugs balances the mean arterial pressure, the cardiac output as well as the peripheral resistances. Therefore, during the cardiac systole, the drugs relax the arterial walls.
Additionally, vasodilators cause the smooth muscle around the blood vessels to relax and this is only achieved when the stimulus that causes the contraction is removed or blocked. The drugs lower the intracellular calcium concentrations thereby permitting the calcium symporters to move the calcium ions making the smooth muscle of the blood vessels to relax
Adverse reaction of the drug
The patient should also be aware of the adverse reactions of the drug. For example, to the central nervous system, the drug causes the confusion, drowsiness, fatigue as well a headache. In other cases it can causes sleep disturbance. On the other hand, chest pain, peripheral edema, as well as blurred vision do occur. Never the less, the drug can cause abdominal pain, anorexia, and indigestion to the GI tract. During respiration, the drug can lead to coughs and difficulty breathing. Finally, it can cause weight gain. Therefore, when the drug is administrated, it is also important to monitors the patient for possible wheezing, breathlessness and cases of asthma attack (Gilmore, Weil, &, Chidsey, 1970, pp. 282:521-527).
Lindmar, R., löffelholz, K. &, Muscholl, E. (1968), a muscarinic mechanism inhibiting the release of noradrenaline from peripheral adrenergic nerve fibres by nicotinic agents. British Journal of Pharmacology and Chemotherapy, 32: 280–294. doi: 10.1111/j.1476-5381.1968.tb00972.x
Michel M, Brodde, E&, Insel P, (1990). Peripheral adrenergic receptors in hypertension. Hypertension.; 16: 107-120. doi: 10.1161/01.HYP.16.2.107
Richard A. Lehne, (2013). Pharmacology for Nursing Care-Pharmacology for Nursing Care. Elsevier Health Sciences.
Gilmore, E, Weil, J, &, Chidsey, C, (1970). Treatment of Essential Hypertension with a New Vasodilator in Combination with Beta-Adrenergic Blockade. N Engl J Med 1970; 282:521-527March 5, 1970 DOI: 10.1056/NEJM197003052821001
Barcelos, R. C. S.; Benvegnú, D. M.; Boufleur, N.; Pase, C.; Teixeira, A. L. M.; Reckziegel, P. C.; Emanuelli, T.; Da Rocha, J. O. B. T.; Bürger, M. E. (2010). “Short Term Dietary Fish Oil Supplementation Improves Motor Deficiencies Related to Reserpine-Induced Parkinsonism in Rats”. Lipids 46 (2): 143–149. doi:10.1007/s11745-010-3514-0