Effect of banana on cold stress test & peak expiratory flow rate in healthy volunteers

Sarkar, Chayna

Accepted June 21, 1999

The effect of banana on cold stress induced hypertension, peak expiratory flow rate and plasma ACE activity in healthy human volunteers was tested. Systolic blood pressure (P

Key words Angiotensin converting enzyme – banana – blood pressure – heart rate – peak expiratory flow rate

The banana Musa genus (family Musaceae) is reported to be useful in hypertension and other cardiovascular diseases in the indigenous system of medicine in India1,2. The effect of banana feeding on deoxy corticosterone induced hypertension and salt consumption in rats has also been reported3. Pulp of ripe banana (Musa sapientum) supplied daily together with standard food pellets prevented an increase in blood pressure induced by the intramuscular injection of deoxy corticosterone in rats3. Recently it has been reported that ripened nendran variety of banana has the highest (100%) angiotensin converting enzyme (ACE) inhibitory activity (in vitro) followed by poovan (98.22%), rasthali (97.7%) etc., varieties of bananas4. Poovan banana accounts for 70 per cent of the banana crop in this part of the country and it has been found to be highly heat stable and also stable at neutral, extreme acidic and alkaline pH4. ACE inhibitors induced dry cough (5-20% patients) which is mediated by ACE inhibitor induced accumulation of bradykinin in lungs5. However, direct evidence of the effect of banana on hypertension and bronchus is lacking. In view of the above reports, the present study was undertaken to study the effect of banana on cold stress induced hypertension, peak expiratory flow rate (PEFR) and plasma angiotensin converting enzyme (ACE) activity in healthy human volunteers.

Material & Methods

Hippuryl-histidyl-L-leucine (HHL), hippuric acid (HA), diamide and bovine serum albumin were obtained from Sigma Chemical Company, USA. Other reagents were analytical grade commercial chemicals. Blood pressure and peak expiratory flow rate were measured by sphygmomanometer (Elkometer, Anita Industries, New Delhi) and pocket peak flow meter (Ferraris Medical Ltd., London) respectively.

Study design: Eighteen healthy volunteers (14 male and 4 female, aged 25-40 yr) participated in this randomized, prospective, cross over study that comprised two phases. In Phase I, each volunteer received one banana (approx. wt 60-70g) per day for 6 days at 0900 h. All parameters were recorded 1 1/2 h after the last banana intake. In Phase II, the volunteers did not receive any banana treatment. There was a 2 wk interval between Phase I and Phase II of this study. Phase I and Phase II again were divided into two groups banana-1 (at rest), banana-2 (during cold stress) and control-1 (at rest), control-2 (during cold test) respectively. All parameters were recorded by two investigators who were unaware of the treatment groups during the entire period of the study. One blood sample was taken during each phase of study. None of the subjects received any vasoactive or non steroidal anti-inflammatory agents throughout the week-long study. Volunteers abstained from taking alcohol for 24 h and also from caffeine containing drinks (tea, coffee), foods and cigarettes for at least 3 h before an^> measurement was taken. Written informed consent was obtained from each subject. All studies were performed between 0900 and 1100 h in a quiet room maintained at a constant temperature (22-25 deg C).

Cold stress test: Volunteers were made to lie in bed comfortably for 10 min. Blood pressure (BP) and heart rate (HR) were recorded every 2 min till three consecutive readings were almost the same and the mean of the three readings was taken as basal BP and HR. The volunteer was then made to put his/her dominant hand up to the wrist in a bucket full of ice cold water at 0?C for 40 sec. At the end of 30 sec, the inflation of the cuff of the sphygmomanometer was started and BP and HR were recorded with the hand still in cold water. The point of disappearance of the fifth Korotkoff sound was taken as diastolic pressure. The first appearance of clear repetitive tapping sound was taken as systolic blood pressure. These parameters were re-recorded every 2 min till they returned to normal.

Peak expiratory flow rate (PEER): The subjects were asked to blow air out of their fully inflated lungs as rapidly as possible and the peak flow rate achieved was recorded with a pocket peak flow meter. The average of three readings was taken as basal PEFR (1/min).

Plasma ACE activity measurement: Human serum ACE activity was measured with hippuryl-L-histidyl-L– leucine (HHL) as substrate by a method modified from Cushman and Chenung6. The reaction mixture (0.175 ml) contained 0.1 ml of SmM HHL dissolved in 0.2 M phosphate buffer pH 8.3 containing 0.6 M NaCl, human serum and distilled water. The human serum in a volume of 50 (mu)l or less was used to initiate the reaction. After 30 min incubation at 37 deg C the reaction was arrested by adding 0.175 ml of I (M) HCl. Hippuric acid was extracted with ethyl acetate, dried and resuspended in ethanol and measured spectrophotometrically at 228nm as described earlier7. One unit of ACE was defined as the amount of enzyme catalyzing the release of I n M of hippuric acid from HHL/min at 37 deg C.

Statistical analysis was done by paired Student’s ‘t’ test.

Results & Discussion

The effect of banana on blood pressure and heart rate at rest and during cold stress in the healthy volunteers is shown in the Table. Systolic BP (P

ACE inhibitors have well established clinical benefits in patients with hypertension, myocardial infarction and congestive heart failures. The ACE inhibiting activity of different bananas has been reported in in vitro studies4. Poovan bananas have high ACE inhibitory activity (98.22%) in vitro, and it was found to be highly stable in heat, acidic, neutral and alkaline pH4. Our results indicate that banana (poovan) inhibits plasma ACE activity in healthy volunteers. The inhibition of plasma ACE activity was about 16-17 per cent which has been shown by others to be adequate to decrease blood pressure in hypertensive patients9.

The pharmacological actions of ACE inhibitors are believed to be mediated by the systemic inhibition of the renin angiotensin system or due to direct vasodilator effect10. Banana may decrease blood pressure by inhibition of plasma ACE activity, especially during cold stress. Cold stress induces a rise in blood pressure by activation of the sympathetic nervous system11. and angiotensin II also interacts with the sympathetic system by facilitating its release12 or inhibiting the reuptake of sympathetic nerve terminals13 or potentiating the post synaptic responsiveness to norepinephrine14,15. Banana through its ACE inhibitory activity may attenuate the effect of norepinephrine during stress and decreases the blood pressure during cold stress. Banana also decreases the systolic blood pressure during rest (not significantly). This may be explained by the ACE inhibitor inducing direct (local effect) vasodilation10.

ACE inhibitors may induce dry cough and bronchoconstriction which are mediated by the accumulation of bradykinin in the lungs5. Our results indicate that there was a slight decrease of peak expiratory flow rate (not significant); so banana may cause negligible or no bronchoconstriction. Further studies are however needed to confirm this finding. The property of banana of decreasing blood pressure during cold stress may be utilized in clinical situations, and banana may be used with benefit as an adjuvant in hypertension therapy. A planned clinical trial using banana in hypertensive individuals is therefore worthwhile.


1. Sastri BN, editor. The wealth of India, vol. VI. New Delhi: Council of Scientific and Industrial Research; 1962 p. 467. 2. Ambasti SP, editor. The useful plants of India. New Delhi: Council of Scientific and Industrial Research; 1986 p. 386. 3. Perfumi M, Massi M, De Caro G. Effect of banana feeding on deoxycorticosterone induced hypertension and salt consumption in rats. Int J Pharmacol 1994; 32:115-25.

4. Rao NM, Prasad KVSRG, Pai KSR. Angiotensin converting enzyme inhibitors from ripened and unripened bananas. Curr Sci 1999; 76: 86-8.

5. Israili ZH, Hall WD. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review

of the literature and pathophysiology. Ann Intern Med 1992; 17: 234-42.

Cushman DW, Chenung HS. Spectrophotometric assay and properties of the angiotensin converting enzyme of rabbit lung.

Biochem Pharmacol 1971; 20:1637-48.

7. Udupa EGP, Rao NM. Distribution and some properties of sheep (Ovis aries) angiotensin converting enzyme. Biochem Mol Biol Int 1993; 31: 851-60.

8. Materson BJ, Preston RA. Angiotensin converting enzyme inhibitors in hypertension. Arch Intern Med 1994;154: 513-23. 9. Gavras H, Biollaz J, Waeber B, Brunner HR, Gavras 1, Davies RO. Antihypertensive effect of the new oral angiotensin converting enzyme inhibitor “MK-421”. Lancet 1981; ii: 543-7. 10. Zarnke KB, Feldman RD. Direct angiotensin converting enzyme inhibitor-mediated venodilation. Clin Pharmacol Ther 1996; 59: 559-68.

11. Chrousos GP, Gold PW. The concepts of stress and stress system disorders: Overview of physical and behavioural homeostasis. JAMA 1992; 267:.1244-52.

12. Starke K. Regulation of noradrenaline release by presynaptic receptor systems. Rev Physiol Biochem Pharmacol 1977; 77: 1-124.

13. Khairallah PA. Action of angiotensin on adrenergic nerve endings: inhibition of norepinephrine uptake. Fed Proc 1972; 31: 1351-7.

14. Lang CC, Rahman AR, Balfour DJK, Struthers AD. Enalapril blunts the antinatriuretic effect of circulating noradrenaline in

man. J Hypertens 1993;11: 565-71.

15. Zimmerman BG, Sybertz EJ, Wong PC. Interaction between sympathetic and renin angiotensin system. J Hypertens 1984; 2: 581-7.

Chayna Sarkar, K.L. Bairy, N.M. Rao* & E.G.P. Udupa*

Departments of Pharmacology & *Biochemistry, Kasturba Medical College, Manipal

Reprint requests: Dr K.L. Bairy, Professor and Head, Department of Pharmacology, Kasturba Medical College, Manipa; 57619

Copyright Indian Council of Medical Research Jul 1999

Provided by ProQuest Information and Learning Company. All rights Reserved

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