Talk about Pharmacy Practice and Therapeutics.
The kidney plays a significant role in controlling blood pressure and managing body fluids.
Studies in the past have shown that hypertension can be caused by disruptions in the functioning of the kidney system.
The main factors that lead to hypertension are: renal arterial vasoconstriction by increased angiotensin I, functional augmentation of the renal vascular tone, elevated renal resistance, and renal arterial vasoconstriction by increased angiotensin 2. Deficit in control of renal bloodflow like decreased renal bloodflow, increased sympathetic activity due to an increase in noradrenalin. An altered response of angiotensin 2 to the renal vasculature results in vasoconstriction
A change in renal vascular tone can cause vascular resistance, and consequently an increase in blood pressure.
The abnormal sympathetic system response to an increase in sodium levels is what causes the alteration in the vascular tone. This is caused by the release of more aldosterone hormones.
Hypovolemia is characterized by decreased blood flow. This is detected by barorecptors located in blood vessels, macula diesa cells in the loop-of-henle and the sympathetic nervous system.
The renal ischemia is caused by a decrease in blood flow.
The juxtaglomerular apparatus’s granular cells release more rennin when they are stimulated by sympathetic stimulation such as an increase in noradrenaline.
Renin senses changes in renal perfusion pressure by using stretch receptors in the renal vessels walls.
Angiotensin II is an adrenal gland hormone that secretes aldosterone. This causes tubular Na+ Cl reabsorption and K+ expulsion, which in turn leads to an increase in blood pressure.
Angiotensin II works on the AT1 receptor, which releases Ca++. This results in a decrease of cAMP, and an increase in blood pressure (Holechek 2003).
Raynaud syndrome affects the extremities of the body, such as fingers and toes.
The condition causes extreme pain and can cause color changes in the extremities.
Extreme conditions such as very high or low temperatures and emotional stress can cause this painful condition.
These external factors can cause narrowing of blood vessels in the extremities.
This is also a result of rheumatoid, lupus, and scleroderma (Marshall, et al. 1976).
Peripheral arterial disease is a complication of your circulatory system. It occurs because there is less blood flow to the heart, limbs and brain from narrowed arteries.
Claudication is also known as pain in the legs.
Atherosclerosis, which is the accumulation of plaque in the blood vessels, caused the narrowing of the arteries.
Plaque is made up of fat, cholesterol, fat, and fibrous tissue.
Peripheral arterial disease can lead to other cardiovascular diseases such as stroke, heart attack, heart disease, and coronary heart disease.
Beta blockers are used primarily for cardiovascular diseases such as hypertension, coronary artery disease and arrhythmias.
This is because both beta 1 and beta 2 receptors are antagonistic in these conditions.
These beta blockers can cause reduced cardiac output and increased alpha adrenergic activity.
This results in reduced blood supply to extremities and vasoconstriction.
Both Raynaud’s disease and peripheral artery diseases cause vasoconstriction, which raises blood pressure. There is also a reduced blood supply to the extremities, such as figures, feet, and limbs.
This can lead to painful conditions like claudication.
These patients may experience a worsening of their disease conditions due to beta blockers.
There are evidences that beta blockers may have caused an increase in the frequency of Raynaud’s syndrome and peripheral arterial disease (Paravastu, et al. (2013)).
Airway remodelling involves injury to epithelial cells, goblet-cell hyperplasia, nucus secretion and subepithelial layers thickening, smooth muscle hyperplasia, and angiogenesis.
Many receptor tyrosine kinases, including epidermal growth factors receptor (EGFR), platelet derived growth factor receptors (PDGFR), and vascular endothelial grow factor receptors (VEGFR), are involved in airway remodeling.
These growth factors are the main binding partners for these kinase enzymes. They play an important role in remodeling the lung in respiratory disease.
These growth factor inhibitors showed reduced collagen deposition, decreased goblet cell proliferation, and reduced smooth muscle contraction in the airways (Manuyakorn, et al. 2013, 2013).
Biological therapies such as Omalizumab and Mepolizumab or Etanercept.
The inflammatory cytokines are responsible for lung diseases.
Patients with lung disease experience an increase in inflammatory cytokines, which leads to airway remodeling.
It is well-established that the epithelium plays a significant role in the initiation of airway remodeling.
These cytokines, as well as environmental factors, can cause epithelium mesenchymal transform (EMT). It must be stopped.
These biological therapies block these cytokines, which in turn prevents EMT maintenance.
These biological therapies aid in the relief of airway remodeling by inhibiting eosinophils’ recruitment and angiogenesis, by preventing smooth cell differentiation, and by acting upon endothelial and alveolar macrophages.
The positive effects of biological therapies on airway remodeling can be seen in the reduction of forced expiratory volume (FEV1) and asthma exacerbations (Cho 2001).
Inhaled corticosteroids: These corticoids, which include flunisolide and budesonide as well as fluticasone, fluticasone, and beclomethasone, are mainly used to treat respiratory conditions like asthma and chronic obstructive pulmonary diseases (COPD).
The main causes of structural airway changes are the cytokines and inflammation cells.
Inhaled corticosteroids cause angiogenesis to be reduced in the lamina propria beneath the epithelium, which in turn results in airway remodeling.
The inhaled corticosteroids had an effect on the remodeling of the airways by reducing bronchial hyperresponsivness. (Riccioni and al., 2004).
Recent advancements in the treatment and mechanisms of asthma airway remodeling: A message from the bench to the clinic
Korean Journal of Internal Medicine 26(4), 367-383.
An overview of renal hemodynamics.
Marshall, A.J. and Roberts, C.J. (1976).
Raynaud’s phenomenon is a side effect of beta blockers in hypertension.
British Medical Journal, 19(1): 1498-1499.
Manuyakorn (W.), Howarth, P.H. and Holgate S.T.
Novel therapy and airway remodeling in asthma.
Asian Pacific Journal of Allergy and Immunology 31, 3, 10.
Paravastu S.C. Mendonca D.A. and Da Silva A.
Beta-blockers for peripheral arterial disease.
Cochrane Database of Systematic Reviews, 11(9) CD005508.
Inhaled antileukotrienes or corticosteroids for the pharmacological treatment of airway remodelling.
Annals of Clinical & Laboratory Science 34(2): 138-142.