Vasopressors are used to explain drugs that constrict blood vessels and increase blood pressure. That is the simple term in which I can explain it, and I am sure you got it. There are different groups of vasopressors, and I will be doing justice to discussing them in this post. Join me as I continue, and I hope you enjoy it.
The first set of vasopressors I will be mentioning are Inodilators with Ino being related to the heart (as in Inotropic which has to do with the increase in contraction of the heart) and the dilator has to do with the dilation of the peripheral vessels. These drugs include Dobutamine which is a beta-agonist binding to Beta 1, 2, and 3 receptors with no alpha-agonistic binding, Milrinone is another drug that inhibits the phosphodiesterase type 3 enzyme, while the third one in this class is Isoproterenol which is a strong beta-agonist.
Dobutamine stimulates the beta receptor which is found on the Atrioventricular nodal system, Sinoatrial nodal system and the contractile myocardium of the heart. A stimulation of the nodal cells causes an increase in the actions of the cells by putting calciums into it which would then increase heart rate known as increased chronotropic activity which will also increase the cardiac output of the heart. Just like I said that there are beta 1 receptors on the contractile myocardium and the stimulation of the beta receptor would lead to an increase in contractility which ultimately causes an increase in stroke volume which increase the cardiac output of the heart. Then Dobutamine do not have any alpha 1 activity causing a vasodilation effect in the vessels, decreasing systemic vascular resistance, thereby decreasing blood pressure. Remember, Alpha 1 receptors causes vaso constriction while Beta 2 receptor causes vasodillation, so with Dobutamine, there will be a vasodilatory effect where there will be a lowering of the systemic vascular resistance and so lowering the blood pressure thereby decreasing the after load of the heart.
With the explanation of the Beta 1 receptor, Isoproterenol activity has been explained. Isoproterenol is a primary beta agonist where there will be an increased heart rate, increase contractility, increased stroke volume, cardiac output increase, it would also cause vasodilation, causing a decrease in afterload, causing a decrease in blood pressure.
Milrinone on the other hand, has its mechanism not similar to the first 2. Its mechanism happens both in the cardiac muscle and in the smooth muscle as a result of adenylate cyclase which converts ATP to Cyclic AMP which stimulates protein kinase A. The effect of protein Kinase A differs depending on the tissue. In the cardiac muscle, it induces the contractility of the cardiac muscle, thereby stimulating the contraction of the muscle. While it causes contractility in the cardiac muscle, it causes a relaxation in the smooth muscle. If the cardiac muscle contract, it would cause an increase in the stroke volume and then increase the cardiac output but then it would cause the smooth muscles to vasodilate leading to a decrease in the systemic vascular resistance causing a reduction in blood pressure and afterload. In the heart, the enzyme Phosphodiesterase type 3 inhibits cyclic AMP but with Milrinone, the enzyme Phosphodiesterase type 3 is inhibited thereby increasing the amount of cyclic AMP which would keep stimulating protein kinase A. Using Milrinone, and Dobutaminecan be useful in people with low cardic output, leading to a cardiogenic shock as it would cause the myocardium to contract more, thereby increasing the cardiac output but then reducing the afterload as it will vasodilate the peripheral vessels.
Inopressors is another category of vasopressors. has to do with the Inotropic, which includes increase heart activities like increased contractility, increased stroke volume, and increased cardiac output, which then leads to increased blood pressure. The pressor there has to do with the lowering of the peripheral vessel, increase syetem vascular resistance, increased blood pressure, and increased afterload. In this category are drugs Norepinerphrine, Epinephrine, and Dopamine.
Norepinerphrine as a drug has a strong alpha 1 receptor agonist activity, and a beta 1 receptor agonist activity. Epinerphrineon lower dose is a strong beta receptor agonist but on higher doses, it becomes an alpha 1 receptor agonist while still being a beta receptor agonist.
Both Norepinephrine and epinephrine stimulate alpha 1 receptors which are present on arterioles and venules and they produce two different effects. On arterioles, it clamps down on the arteries causing an increase in the systemic vascular resistance, increase in blood pressure and after load. On venules, it would lead to an increase in the vasoconstriction of the venules, thereby causing more blood to get into the right side of the heart increasing the preload of blood from the heart, thereby increasing stroke volume of the heart, and the cardiac output of heart.
For Beta receptor, I discussed it previously. Epinerphrine is a beta argonist, causing bronchodilation, inhibiting mast cell from releasing histamine which would have caused bronchospasm, and it acts on the liver to increase the production of lactate. Patients with septic shock, and patient with cardiogenic shock which lead to a low cardiac output can be treated with norepinerphrine and epinerphrine.
Doparmine on lower doses it give a dopamine receptor activity type and this can lead to an increase in cardiac output and a decrease in systemic vascular resistance and it can lead to hypotension. It stimulates the beta receptor activity depending on the dose.
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