Moxonidine is a second-generation, centrally acting antihypertensive drug with a distinctive mode of action. Moxonidine activates I1-imidazoline receptors (I1-receptors). Imidazoline I1-receptor agonism represents a new mode of antihypertensive action to inhibit peripheral alpha-adrenergic tone by a central mechanism. Adrenaline, noradrenaline and renin levels are reduced, a finding consistent with central inhibition of sympathetic tone. Moxonidine acts centrally to reduce peripheral sympathetic activity, thus decreasing peripheral vascular resistance. In patients with mild to moderate hypertension, moxonidine reduces blood pressure (BP) as effectively as most first-line antihypertensives when used as monotherapy and is also an effective adjunctive therapy in combination with other antihypertensive agents. It improves the metabolic profile in patients with hypertension and diabetes mellitus or impaired glucose tolerance, is well tolerated, has a low potential for drug interactions and may be administered once daily in most patients. Moxonidine is a good option in the treatment of patients with mild to moderate hypertension, particularly as adjunctive therapy in patients with the metabolic syndrome.

Levosimendan (Simdax) is a novel intravenous agent that exerts inotropic effects through sensitization of myofilaments to calcium and vasodilator effects by binding to cardiac troponin C in a calcium-dependent manner. It also has a vasodilatory effect, by opening adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle to cause smooth muscle relaxation. Unlike other calcium sensitizing compounds, the binding of levosimendan is highly dependent on the intracellular concentration of calcium, such that calcium sensitivity is enhanced only when the calcium level is elevated. Levosimendan is licensed for the treatment of decompensated heart failure in many countries but not in North America. This drug also passed phase III clinical trials for the prevention of low cardiac output syndrome in pediatric patients after open heart surgery.

Meticrane is a diuretic. Meticrane is used to treat essential hypertension.

Guanoclor is an anti-hypertensive agent developed by Pfizer Ltd. (U.K.). It seems to be effective in various types of hypertension (unknown aetiology, renal, and malignant). It affects both systolic blood-pressure and diastolic blood-pressure. It is an adrenergic neurone-blocking agent, which also interferes with noradrenaline synthesis by inhibition of the enzyme dopamine beta-hydroxylase. Clinical use of the compound was first reported by Lawrie et al. (1964), who achieved satisfactory blood-pressure control in 60% of their cases with guanoclor alone, and in a further 18% with the addition of a thiazide diuretic. They also noted a significant reduction in urinary noradrenaline levels during guanoclor administration. Guanochlor has an affinity for the Na+/H+ exchanger ranging between 0.5 uM and 6 uM in different systems and is more potent than amiloride in all systems studied. It is suggested that guanochlor recognizes a binding site on the Na+/H+ exchanger that is distinct from the amiloride binding site.

Guanoxabenz is an antihypertensive drug that was in clinical use in the 1980s. It acts as a selective agonist of alpha2A1 and alpha2B1 adrenergic receptors. Guanoxabenz is the main metabolite of the FDA-approved drug guanabenz.

Endralazine (6-benzoyl-3-hydrazino-5,6,7,8-tetrahydropyrido-(4,3-c)-pyridazine mesylate) is a peripheral vasodilator drug, which acts by direct relaxation of the smooth muscle fibres of the peripheral arterial vessels. Endralazine has been used as an antihypertensive agent.

Benziodarone is a coronary dilatator drug. Benziodarone in therapeutic dosage has no effect on blood coagulation and does not alter the prothrombin level. Bleeding complications occurred, when benziodarone is given to patients receiving anticoagulant therapy with warfarin sodium. Jaundice might occurred from 8 to 16 weeks after the beginning of the treatment with Benziodarone. Combination of Flecainide with Benziodarone should be avoided or used only with strict monitoring. Benzbromarone is an other benzofuran derivative acting as anuricosuric agent by reducing the proximal tubular reabsorption of uric acid. The hypouricaemic action of benziodarone (Amplivex-Labaz) is prompt. The maximum drop of uricaemia after Amplivex administration (2 tablets/day) occurs during the first three days. The uric acid level declines by as much as 80% of the baseline value. For long-term treatment 1 tablet per day is sufficient, in some instances even 1 tablet twice a week. The tolerance of the preparation is satisfactory.

Ronifibrate, a hypolipidemic agent, is an agonist of peroxisome proliferator-activated receptor.

Bietaserpine is a derivative of a Rauwolfia alkaloid reserpine. It was used as an antihypertensive agent and marketed in the 1960s in France and Italy. Bietaserpine is believed to act by inhibiting VMAT receptors.

Acipimox (5-methylpyrazinecarboxylic acid 4-oxide) is a new lipolysis inhibitor that has a distant chemical relationship with nicotinic acid (NA). The anti-lipolytic action of acipimox is mediated through suppression of intracellular cyclic AMP levels, with the subsequent decrease in cyclic AMP-dependent protein kinase activity, leading to the reduced association of hormone-sensitive lipase with triacylglycerol substrate in the lipid droplet of adipocytes. Acipimox has been identified as an agonist at G-protein coupled nicotinic acid HM74A and HM74B receptors. Acipimox (Olbetam) is indicated for the treatment as alternative or adjunct treatment to reduce triglyceride levels in patients who have not responded adequately to other treatments such as statin or fibrate treatment for hypertriglyceridaemia (Fredrickson type IV hyperlipoproteinaemia) and hypercholesterolaemia and hypertriglyceridaemia (Fredrickson type IIb hyperlipoproteinaemia).