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PubMed1975

Current therapy of hypertension. A pharmacologic approach.

Adequate treatment of hypertension requires that the physician understand the pharmacologic actions of antihypertensive agents. Although no drug is without adverse reactions, it should be possible to choose an agent or combination of agents which can effectively lower blood pressure and be tolerated by the patient. The indications, proposed mechanisms of actions and adverse effects of the following antihypertensive drugs are discussed: thiazide diuretics, spironolactone, triamterene, trimethaphan, Rauwolfia alkaloids. guanethidine, bethanidine, methyldopa, clonidine, pargyline, propranolol, hydrazaline, minoxidil, guancydine, diazoxide and sodium nitroprusside.

Adrenergic alpha-Antagonists↗
PubMed1975

Adverse reactions and interactions limiting the use of antihypertensive drugs.

One major problem in the management of hypertensive patients is their lack of compliance with therapeutic regimens. Some of the problem with compliance is due to side effects of the drugs being used. Additionally, drug resistance may be related to interactions of antihypertensive drugs with other prescription and nonprescription drugs. By classifying drugs into common modes of action, common side effects can be predicted. However, each drug has its own spectrum of other side effects which can be dose-limiting. Most of the side effects are extensions of the pharmacologic actions of these drugs, and only relatively rarely is an allergic reaction a problem. Drug interactions can be important in explaining some side effects or drug resistance. A knowledge of the pharmacology of the antihypertensive drugs allows the physician to predict, in many cases, the possibility of an interaction and, indeed, can allow the use of interactions to advantage as with combinations of vasodilators and beta adrenergic blocking drugs. Until such time as the perfect antihypertensive drug is discovered, most patients can be managed satisfactorily with minimal side effects by judicious combination of available drugs and avoiding drugs which interact to cause more side effects or decrease the antihypertensive effects.

Antihypertensive Agents↗
PubMed1992

Identification of muscarinic acetylcholine receptors in isolated canine lingual epithelia via voltage clamp measurements.

Acetylcholine (ACh), muscarine and methacholine all decreased the short-circuit current (Isc) measured across isolated canine lingual epithelia bathed in symmetrical solutions of Krebs-Henseleit buffer when added to the serosal, but not mucosal, solutions. Atropine inhibited the ACh-induced decrease in Isc whereas serosal solutions of 1 mM hexamethonium or 1 mM nicotine did not. Addition of a membrane-permeable analogue of cAMP also reduced Isc and, in the presence of this analogue, the decrease in Isc produced by ACh was markedly reduced. These data suggested the presence of muscarinic acetylcholine receptors in the serosal membranes of isolated canine lingual epithelia. The decrease in Isc induced by ACh may involve the inhibition of Ba(2+)-inhibitable K+ currents, as the addition of 100 microM BaCl2 to the serosal solution inhibited Isc and also completely inhibited the response produced by ACh. These findings suggest that responses of sensory fibres in lingual epithelia elicited by ACh may involve an interaction of ACh with epithelial cells rather than a direct interaction of ACh with receptors on sensory nerves.

Acetylcholine↗
PubMed1983

Kappa-bungarotoxin: a probe for the neuronal nicotinic receptor in the avian ciliary ganglion.

The interaction of snake alpha-neurotoxins with neuronal membranes has been examined in the chick ciliary ganglion. Some, but not all, alpha-neurotoxins block nicotinic transmission in this ganglion. alpha-Bungarotoxin (ABgT), the major alpha-neurotoxin in the venom of Bungarus multicinctus, does not block transmission at high concentrations (1.2 microM) although it binds (Kd = 1 nM) to a pharmacologically nicotinic site in the ganglion. A toxin (kappa-bungarotoxin, KBgT) has been purified from the venom of Bungarus multicinctus. KBgT has a molecular weight of 6500 daltons and a pI of 9.1. KBgT is a potent inhibitor of nicotinic transmission in the ciliary ganglion, producing a reversible (overal several hours) blockade at 75 nM. Pre-exposure of ganglia to 1.2 microM ABgT does not prevent the effects of KBgT, indicating that the blockade occurs at a site distinct from that recognized by ABgT. Binding of [125I]KBgT to ciliary ganglia reveals two binding sites: one which has previously been characterized by [125I]ABgT and one which is not identified by [125I]ABgT. Both of these [125I]KBgT binding sites are blocked following pre-treatment of ganglia with the irreversible nicotinic affinity agent bromoacetylcholine. A two-site model is proposed to account for these observations. One site (the ABgT binding site) is seen by both ABgT and KBgT, and has as yet no physiological function associated with it. The second site is recognized only by the physiologically active KBgT, and may represent binding of the toxin to the physiologically detected nicotinic receptor.

Acetylcholine↗
PubMed1990

Spinal mediation of the increases in arterial pressure and heart rate in response to intrathecal administration of bicuculline.

The present experiments were designed to determine the mechanisms by which the intrathecal administration of the GABAA antagonist, bicuculline (2.2 and 8.8 nmol), at the second thoracic spinal segment (T2) affects cardiovascular function in the anaesthetized rat. Bicuculline produced a dose-related, transient increase in arterial pressure and heart rate which peaked at 5-7 min and persisted for 30 min or more, depending on dose. There was a mutually reversible interaction between bicuculline and intrathecal administration of the GABAA agonist, muscimol (8.8 nmol), which alone decreased arterial pressure and heart rate. Bicuculline was given intrathecally at the third lumbar spinal level (8.8 nmol) and intravenously (8.8 nmol), but in these cases it failed to affect these cardiovascular parameters. Pretreatment with intrathecal infusion of 15 microliters of 1% lidocaine or with intravenous injection of hexemathonium (10 mg/kg) prevented the responses to intrathecal administration of 8.8 nmol of bicuculline at T2. These results demonstrate that the effects of bicuculline on arterial pressure and heart rate are due to an action in the spinal cord on GABAA receptors, and the data may be interpreted as indicating that there is a tonic GABAergic inhibition of sympathetic outflow at the spinal level.

Animals↗
PubMed1991

Sympathetic inhibition and attenuation of spontaneous hypertension by PVN lesions in rats.

To determine whether the paraventricular nucleus (PVN) contributes to the development of hypertension in spontaneously hypertensive rats (SHR), we compared cardiovascular responses to ganglionic blockade with hexamethonium or vasopressin antagonism with dPVAVP in sham-operated or PVN lesioned SHR and Wistar-Kyoto rats (WKY). Lesions were produced electrolytically when the rats were 5 weeks old. During the next 3 weeks, tail-cuff measurements showed that the development of hypertension in SHR was inhibited, while systolic pressure in WKY was unaffected. Mean pressures recorded directly from the femoral artery at 8 weeks of age were lower in lesioned than in sham-operated SHR (141 +/- 5 vs 110 +/- 3 mm Hg, P less than 0.05), but did not differ in corresponding WKY groups (110 +/- 4 vs 112 +/- 5 mm Hg). Depressor responses to ganglionic blockade induced by i.v. injection of hexamethonium (25 mg/kg) were significantly larger in sham-operated than in lesioned SHR (-41 +/- 4% vs -28 +/- 3%, P less than 0.05). By contrast, vasopressin antagonism with dPVAVP did not alter blood pressure in all rat groups. In 24-h urine samples, excretion of vasopressin was unaffected, but that of norepinephrine was significantly reduced in lesioned SHR. These findings suggest that the PVN contributes to the development of spontaneous hypertension by sympathetic activation without increasing vasopressin secretion.

Animals↗