Hypertension is another term used for high blood pressure, where it is measured in pressure units and typically found in patients at 160mmHg/100mmg. It is measured at the systolic and diastolic. The hyperlipemia is combined with the hypertension, where it is known as a high lipid/cholesterol count, where the LDL levels are at 2mmol/L are known as a high risk. The key drugs available for this are either Thiazide diuretics, b1- adrenoreceptors antagonists and ACE inhibitors which would work alongside the HMG-Coa reductive inhibitors.
The thiazide diuretics acts on the distal tubule of kidney at the point of transition of water and salts, where the site of action is on the specific transporter proteins allowing the reabsorption of salts from the tubule to the bloodstream. Which have hormonal and therapeutic control points. The thiazide drug binds to the C1 transporter, also known as the Cl- binding site of the sodium chloride co transporter system, which essentially means there will no longer be the binding of the chloride ions, which the inhibit the salt reabsorption into the bloodstream. The blood volume will decrease, since there is no uptake of water and salt as the water will remain in the distal tubule due to the retention of the osmotic balance, which means it will be excreted. Hence, the side effect of frequent urination. The thiazides have effects of having vasodilator action on the vascular tissue, regulating the Ca+ ions and reducing the blood volume in the increased renin secretion
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Another drug to treat hypertension is β1- adrenoceptor antagonists, which is situated on the cell membranes of cardiac, intestinal, bronchial, and vascular smooth muscle. The endogenous neurotransmitter ‘noradrenaline’ activates the β1- adrenoceptor, which is released from the post ganglionic nerve terminal. This will then activate the GPCR mediated pathway and adenylyl cyclase pathway by interacting with the GPCR on the cardiac cell. To be able to increase the likelihood of the channel opening there should be a phosphorylation by protein kinase A, on the alpha 1 subunit of the calcium ion channels, which are on the cardiac cell membrane. The bioavailability of the intracellular calcium ions will increase, leading to the increased rate and force of contraction. There are also nonselective versions of the β1- adrenoceptor antagonists like propanol, which can have an effect on asthmatics as it causes bioconstruction due to the sympathetic nerves which have innervated on the bronchioles which typically activate the β2 adrenoreceptors that promote bronchodilation. The selective agents like atenolol are concentration dependent. When the selective β1 receptors have a high concentration or dosage they are found to be poor in intact cells and then β1 selective actually have a higher affinity for the β2 adrenoreceptors, hence why there needs to be more development of selective β-antagonists. Both examples have a level of cross reactivity, which makes an effect on the drug development.
Using ACE inhibitors is also an additional drug that you can use to treat hypertension. On the vascular endothelium, the carboxypeptidase ACE cleaves the C-terminal pair of amino acids from the peptide precursors. In order for ACE activity, there is a zinc ion in the active site, the ACE inhibitors will also mimic this same peptide structure ensuring it is stable and still has the absorption properties, however the ACE inhibitors will block the active site and via the sulfhydryl group, there will be reversible binding to the zinc ion and which is normally occupied on the C-terminal leucine of angiotensin I, so proline residue will bind to the site normally. The ACE target degrades ACE to angiotensin II and bradykinin, so it does not accumulate in the bronchial tissues when undergoing ACE inhibitor therapy. The possible option for drugs is Captopril (1ST generation) and Lisinopril. Alongside the ATI receptor antagonists like Losartan, which is newly developed and prevent angiotensin II binding to the ATI receptor, preventing a dry cough which they could possibly get when using the other drugs, however it is still considered as a second choice.
Statins like HMG-Coa reductase inhibitors are used to treat hyperlipidaemia, by inhibiting the rate limiting step of the cholesterol synthesis, converting HMG-Coa to mevalonic acid, subsequently reducing the amount of cholesterol. There is then an increase in LDL uptake as more LDL receptors are presented on the cell surface, overall leading to a decrease of cholesterol in the blood. They cause partial inhibition of the enzyme and impair the synthesis of the isoprenoids which are vital for cellular functions. The reductase inhibitors induce an increase in high affinity of LDL receptors. Options of drugs that could be used are simvastatin, lovastatin, and atorvastatin.
In conclusion, for combined hypertension and hyperlipidaemia it is clear that there should be a dramatic lifestyle changes, like diet change. However, there are an option of 3 drugs for hypertension which needs to be taken alongside HMG-Coa reductase inhibitors.
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