In the US, Ethaverine is a member of the drug class peripheral vasodilators. It’s an alkaloid prepared synthetically from opium with no narcotic properties. Directly relaxes all smooth muscles, especially when they have been spasmodically contracted. Action is especially pronounced when spasm is present on coronary, cerebral, pulmonary, and peripheral arteries. Acts directly on myocardium like quinidine; depresses conduction and irritability, and prolongs refractory period. Primarily for peripheral and cerebral vascular insufficiency associated with arterial spasm; also a smooth muscle spasmolytic in spastic conditions of the GI and GU tracts. Adverse Effects ( 1%) CNS: Vertigo, headache, drowsiness. CV: Hypotension, arrhythmias. GI: Nausea, anorexia, abdominal distress, dry throat. Other: Malaise, flushing, sweating, lassitude, respiratory depression. Ethaverine may decrease levodopa effectiveness; morphine may antagonize smooth muscle relaxation effect of ethaverine.

Anhydrous dibasic calcium phosphate is a calcium salt of phosphoric acid. It is used as a diluent in pharmaceutical industry, in some toothpastes as a polishing agent. Calcium phosphate is generally recognized as safe by FDA. Dibasic calcium phosphate is ised as a supplement to treat conditions associated with calcium deficit, such as bone loss (osteoporosis), weak bones (osteomalacia/rickets), decreased activity of the parathyroid gland (hypoparathyroidism), and a certain muscle disease (latent tetany)

Broparestrol, (Z)- is an isomer of Broparestrol -- synthetic, nonsteroidal selective estrogen receptor modulator (SERM) of the triphenylethylene group that has been used in Europe as a dermatological agent and for the treatment of breast cancer. Broparestrol, (Z)- and Broparestrol, (E)- demonstrates antiestrogenic activity but, unlike broparestrol, were never marketed.

Indenolol hydrochloride is a nonselective beta-adrenoceptor antagonist. It is antihypertensive, antiarrhytmic, antianginal drug. It vasodilated forearm arterioles and this effect was antagonized by beta-blockade, thus demonstrating vascular intrinsic sympathomimetic activity. Indenol is able to inhibit an exercise-induced rise in systolic pressure. Indenolol would be able to decrease myocardial O2 consumption.

Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up. Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. Angiotensin I is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells and kidney epithelial cells). ACE found in other tissues of the body has no physiological role (ACE has a high density in the lung, but activation here promotes no vasoconstriction, angiotensin II is below physiological levels of action). Angiotensin II acts as an endocrine, autocrine/paracrine, and intracrine hormone. Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and stimulation of PAI-1 and PAI-2. When cardiac cell growth is stimulated, a local (autocrine-paracrine) renin-angiotensin system is activated in the cardiac myocyte, which stimulates cardiac cell growth through protein kinase C. The same system can be activated in smooth muscle cells in conditions of hypertension, atherosclerosis, or endothelial damage. Angiotensin II is the most important Gq stimulator of the heart during hypertrophy, compared to endothelin-1 and α1 adrenoreceptors. Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers. Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle. Angiotensin II has a direct effect on the proximal tubules to increase Na+ reabsorption. It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting. Increases in systemic blood pressure will maintain renal perfusion pressure; however, constriction of the afferent and efferent glomerular arterioles will tend to restrict renal blood flow. The effect on the efferent arteriolar resistance is, however, markedly greater, in part due to its smaller basal diameter; this tends to increase glomerular capillary hydrostatic pressure and maintain glomerular filtration rate. A number of other mechanisms can affect renal blood flow and GFR. High concentrations of Angiotensin II can constrict the glomerular mesangium, reducing the area for glomerular filtration. Angiotensin II is a sensitizer to tubuloglomerular feedback, preventing an excessive rise in GFR. Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction. The net effect of these competing mechanisms on glomerular filtration will vary with the physiological and pharmacological environment. Angiotensin was independently isolated in Indianapolis and Argentina in the late 1930s (as 'angiotonin' and 'hypertensin', respectively) and subsequently characterised and synthesized by groups at the Cleveland Clinic and Ciba laboratories in Basel, Switzerland.

Ziconotide (PRIALT; SNX-111) is a neuroactive peptide, which was approved by FDA in 2004 for the management of severe chronic pain in adult patients for whom intrathecal therapy is warranted, and who are intolerant of or refractory to other treatment, such as systemic analgesics, adjunctive therapies, or intrathecal morphine. Ziconotide acts as a selective N-type voltage-gated calcium channel blocker, which leads to a blockade of excitatory neurotransmitter release from the primary afferent nerve terminals.

Bivalirudin is a synthetic 20 amino acid peptide rationally designed based on structural studies of hirudin, a naturally occurring anticoagulant. Bivalirudin is sold under the brand name Angiomax and is indicated for use as an anticoagulant in patients with unstable angina undergoing percutaneous transluminal coronary angioplasty (PTCA). It is intended for use with aspirin and has been studied only in patients receiving concomitant aspirin. Bivalirudin directly inhibits thrombin by binding simultaneously to its active catalytic site and its substrate recognition site.

Indium In-111 is used in specialized diagnostic applications, for example, with indium-111 labelled antibodies. It is useful for labelling blood cell components. Other applications include labelling of platelets for thrombus detection, labelled leukocytes for localization of inflammation and abscesses, as well as leukocyte kinetics. Indium forms a saturated (1:3) complex with oxyquinoline. The complex is neutral and lipidsoluble, which enables it to penetrate the cell membrane. Within the cell, indium becomes firmly attached to cytoplasmic components; the liberated oxyquinoline is released by the cell. It is thought likely that the mechanism of labeling cells with indium In 111 oxyquinoline involves an exchange reaction between the oxyquinoline carrier and subcellular components which chelate indium more strongly than oxyquinoline. Indium In-111 oxyquinoline is indicated for radiolabeling autologous leukocytes. Indium In-111 oxyquinoline labeled leukocytes may be used as an adjunct in the detection of inflammatory processes to which leukocytes migrate, such as those associated with abscesses or other infection, following reinjection and detection by appropriate imaging procedures. The degree of accuracy may vary with labeling techniques and with the size, location and nature of the inflammatory process. Sensitivity reactions (urticaria) have been reported. The presence of fever may mask pyrogenic reactions from indium In 111 oxyquinoline labeled leukocytes. Indium In-111 Chloride is a diagnostic radiopharmaceutical intended for radiolabeling OncoScint (satumomab pendetide) or ProstaScint (capromab pendetide) used for in vivo diagnostic imaging procedures and for radiolabeling Zevalin (ibritumomab tiuxetan) in preparations used for radioimmunotherapy procedures.