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Am J Cardiol. 1990 Nov 15;66(17):1233-6.
Atenolol therapy for exercise-induced hypertension after aortic coarctation repair.

Kavey RE, Cotton JL, Blackman MS.

Division of Pediatric Cardiology, State University of New York Health Science Center, Syracuse 13210.

After successful repair of coarctation of the aorta in childhood, exercise-induced upper body systolic hypertension is well documented. Beta blockade has been shown to reduce the arm/leg gradient in untreated coarctation of the aorta; treatment before coarctation repair has decreased paradoxical hypertension after repair. Ten patients with successful surgical repair of coarctation, defined as a resting arm/leg gradient of less than or equal to 18 mm Hg, were evaluated by treadmill exercise before and after beta blockade with atenolol. Mean age was 5.5 years at repair and 18 at study. At baseline evaluation, systolic blood pressures at termination of exercise ranged from 201 to 270 mm Hg (mean 229 mm Hg). Arm/leg gradients at exercise termination ranged from 30 to 143 mm Hg (mean 84). Follow-up treadmill exercise studies were performed after beta blockade. Upper extremity systolic pressures at exercise termination were normalized in 9 of 10 patients. Maximal systolic blood pressure recorded at exercise termination ranged from 163 to 223 mm Hg (mean 196 mm Hg, p less than or equal to 0.005). Arm/leg gradient at termination of exercise also decreased significantly to a mean of 51 mm Hg (p less than 0.05). No patient had symptoms on atenolol and exercise endurance times were unchanged. The study results in this small series suggest that cardioselective beta blockade can be used to treat exercise-induced upper body hypertension effectively after surgical repair of coarctation. Because a high incidence of premature cardiovascular disease has been well documented after satisfactory surgical repair, the findings are of importance for this group of postoperative patients.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2239728&dopt=Abstract




Br J Pharmacol. 1988 Jun;94(2):609-19.
Involvement of central alpha- and beta-adrenoceptors in the pressor response to electrical stimulation of the rostral ventrolateral medulla in rats.

Ward-Routledge C, Marshall P, Marsden CA.

Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham.

1. Electrical stimulation of the C1 area of the rostral ventrolateral medulla in rats elicits an increase in mean arterial pressure (MAP). 2. This increase in MAP is attenuated by intra-hypothalamic and intracisternal administration of the non-selective beta-adrenoceptor antagonist (+/-)-propranolol and the beta 2-selective antagonist ICI 118551. 3. The selective beta 1-antagonist atenolol and (+)-propranolol, which is inactive on beta-adrenoceptors, did not alter the increase in MAP produced by stimulation of the C1 area. 4. The alpha 2-adrenoceptor antagonist idazoxan enhanced the effects of C1 stimulation on MAP when administered either into the posterior hypothalamus or intracisternally. 5. The results indicate that beta 2- and alpha 2-receptors both have a role in the mediation of the rise in MAP during stimulation of the C1 area and that the receptors involved are located both within the hypothalamus and the spinal cord.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2840166&dopt=Abstract




Basic Res Cardiol. 1986;81 Suppl 1:157-69.
Significance of physical exercise in hypertension. Influence of water temperature and beta-blockade on blood pressure, degree of cardiac hypertrophy and cardiac function in swimming training of spontaneously hypertensive rats.

Vogt M, Ott B, Rupp H, Jacob R.

In previous studies swimming training (ST) of spontaneously hypertensive rats (SHR) at 36 degrees water temperature (WT) led to a decrease in blood pressure (BP). A similar effect of ST has not been described in human hypertension. Our purpose was to investigate the influence of WT on this training effect, the influence of ST on LV hypertrophy and the involvement of adrenergic stimuli in the latter. Male SHR (20 weeks old) were divided randomly into 4 groups. 1) SHR sedentary 2) SHR ST 36 degrees 3) SHR ST 26 degrees 4) SHR ST 36 degrees + atenolol (50 mg/kg/die). ST was performed 2 X 90 min/day for 31 days and then reduced to 2 X 60 min/day. After 7 weeks of ST BP was lower in all ST groups compared with SHR sedentary (p less than 0.001). BP was higher in ST 26 degrees than in ST 36 degrees (p less than 0.05). No additional effect of atenolol on BP was observed. The increase in the degree of LV hypertrophy during ST (ST 36 degrees: +15%; ST 26 degrees: +26%) could be prevented by atenolol (ST 36 degrees + atenolol: -1.5%). ST 36 degrees led to improved ventricular and myocardial performance with decreased LV wall stress ("luxury hypertrophy"), while in ST 26 degrees ventricular dilatation occurred with increased systolic wall stress and elevated LVEDP. It was uncertain whether this should be interpreted as a state of LV pre-insufficiency in ST 26 degrees in spite of no indications of impaired myocardial contractile capability. Peripheral vascular resistance (PVR) was significantly reduced by ST. The reduction was more evident in ST 26 degrees, but was partially compensated for by an increased cardiac output. The weights of adrenal glands increased (p less than 0.001), most markedly for ST 26 degrees. The level of thyroid hormones (T3 and fT3) was increased in ST 26 degrees. In summary, ST proved to be effective in lowering BP of SHR. WT had great influence with respect to cardiovascular adaptation and mechanisms involved in ST of SHR. Cardioadrenergic drive was of great significance for the process of hypertrophy during ST in SHR.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2947562&dopt=Abstract












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