Hypotension antagonists

The cardiac effects of the calcium antagonists, ie, slowed rate (negative chronotropy) and decreased contractile force (negative inotropy), are prominent in isolated cardiac preparations. However, in the intact circulation, these effects may be masked by reflex compensatory adjustments to the hypotension that these agents produce. The negative inotropic activity of the calcium antagonists may be a problem in patients having heart failure, where contractility is already depressed, or in patients on concomitant -adrenoceptor blockers where reflex compensatory mechanisms are reduced. 

The side effects or toxic effects that the calcium antagonists have in common are hypotension, facial flushing, headache, di22iness, weakness, sedation, skin rash, edema, constipation, and abdominal discomfort (nausea, vomiting, and epigastric pressure). 

With most DA agonists there are the other expected signs of increased DA activity such as hallucinations, psychosis and hypotension which can be worse than with levodopa. Fortunately vomiting can be countered by giving the DA antagonist domperidone. This does not cross the blood-brain barrier and so counteracts only the peripheral (chemoreceptor trigger zone) effect of the DA agonist (Fig. 15.5). 

Aldosterone antagonists Hypotension, hyperkalemia, increased serum creatinine BP and HR every shift during oral administration during hospitalization, then once every 6 months baseline SCr and serum potassium concentration SCr and potassium at 48 hours, at 7 days, then monthly for 3 months, then every 3 months thereafter following hospital discharge... 

Apomorphine is approved for acute off episodes in patients with advanced stages of PD. The onset of effect is within 10 to 20 minutes and the duration of effect is about 60 minutes. It requires premedication with an antiemetic because it causes nausea and vomiting. Antiemetics that block central dopamine worsen the symptoms of PD, and 5-HT3 antagonists, such as ondansetron, can aggravate PD-related hypotension. Trimethobenzamide (300 mg three times daily) should be... 

If the patient is started on an a-adrenergic antagonist, monitor the patient for hypotension, dizziness, or syncope. If present, assess the severity of each symptom. Reduce the drug dose or discontinue the drug, as necessary. If the patient has malaise or rhinitis, reassure the patient that these are usual, but bothersome, adverse effect, that often improve with continued therapy. 

Stress ulcer prophylaxis is recommended in septic patients. Patients at greatest risk for stress ulcers are coagulopathic, mechanically ventilated, and hypotensive. Histamine-receptor antagonists are more efficacious than sucralfate, and proton pump inhibitors have not been compared to histamine-receptor antagonists. However, they do demonstrate equivalence in the ability to increase gastric pH.24... 

Mouse vas deferens (MVD) seems to express CB1 and at least one CB2-like cannabinoid receptor type, as is demonstrated by the presence of CB1 and CB2-like mRNA as well as by data collected from experiments with cannabinoid receptor selective agonists and antagonists (Pertwee, 1999). Furthermore, evidence indicates that a CBl-like receptor exists in vascular endothelium, which upon activation produces significant hypotension (Wagner, 1999). This receptor differs from CB1 in its pharmacological response to some well-characterized cannabimimetics. 

Varga KLK, Martin BR, Kunos G. Novel antagonist implicates the CB1 receptor in the hypotensive action of anandamide. Eur J Pharmacol 1995 278 279-283. 

There is evidence that y-aminobutyric acid A receptors may be modified during SE and become less responsive to endogenous agonists and antagonists. Two phases of GCSE have been identified. During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, and hypotension, shock, rhabdomyolysis, secondary hyperkalemia, and acute tubular necrosis may ensue. 

Many different drug classes have shown to cause hypotension and orthostatic reactions and drugs for cardiovascular conditions, psychoactive medicines and polypharmacy, can all have this side effect (Box 5.15). Among the most frequently used drugs in the elderly are diuretics, ACE-inhibitors, angiotensin II antagonists, calcium channel blockers and antidepressants. 

Neurotensin (NT) is a tridecapeptide (Table 4.2) first isolated from brain and gut by Carraway and Leeman [75] and reported by them to induce a rapid and transient hypotension, a cutaneous vasodilatation, and a cyanosis of the extremities in the anaesthetized rat. This report, along with others [76-78] indicating that the NT-induced hypotension and increased vascular permeability could be blocked by histamine receptor antagonists such as mepy-ramine [77] or by pretreatment with compound 48/80 [76], suggested that endogenous histamine (perhaps released from tissue mast cells) was involved in producing some of the biological effects of NT [78]. 

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