Severity of hypertension in familial hyperaldosteronism type I: relationship to gender and degree of biochemical disturbance.

In familial hyperaldosteronism type I (FH-I), inheritance of a hybrid 11beta-hydroxylase/aldosterone synthase gene causes ACTH-regulated aldosterone overproduction. In an attempt to understand the marked variability in hypertension severity in FH-I, we compared clinical and biochemical characteristics of 9 affected individuals with mild hypertension (normotensive or onset of hypertension after 15 yr, blood pressure never >160/100 mm Hg, < or = 1 medication required to control hypertension, no history of stroke, age >18 yr when studied) with those of 17 subjects with severe hypertension (onset before 15 yr, or systolic blood pressure >180 mm Hg or diastolic blood pressure >120 mm Hg at least once, or > or = 2 medications, or history of stroke). Severe hypertension was more frequent in males (11 of 13 males vs. 6 of 13 females; P < 0.05). All 4 subjects still normotensive after age 18 yr were females. Of 10 other affected, deceased individuals (7 males and 3 females) from a single family, all six who died before 60 yr of age (4 by stroke) were males. Biochemical studies were conducted in 6 mild and 16 severe subjects. The 2 groups were similar in terms of urinary sodium excretion. Mild subjects tended, although not significantly, to have lower urinary 18-oxo-cortisol (mean +/- SD, 27.4 +/- 9.0 vs. 35.2 +/- 12.9 nmol/mmol creatinine x day), higher plasma potassium (4.0 +/- 0.3 vs. 3.6 +/- 0.4 mmol/L), and lower recumbent (0800 h after overnight recumbency) plasma aldosterone levels (498 +/- 279 vs. 744 +/- 290 pmol/L). Upright (midmorning after 2-3 h of upright posture) plasma aldosterone levels were similar (mild, 485 +/- 150; severe, 474 +/- 188 pmol/L). In 1 normotensive female, upright PRA was much higher, and the upright aldosterone/PRA ratio was much lower than that in the other subjects. The remaining mild subjects had similar upright PRA levels (mild, 2.8 +/- 1.4; severe, 3.7 +/- 3.2 pmol/ L x min) and aldosterone/PRA ratios (mild, 199.5 +/- 133.4; severe, 200.6 +/- 150.9) as severe subjects. During angiotensin II (AII) infusion studies (n = 6 mild and 10 severe), performed during recumbency, aldosterone levels were lower in the mild group both basally (404 +/- 144 vs. 843 +/- 498 pmol/L; P < 0.05) and after 60 min AII (2 ng/kg x min; 261 +/- 130 vs. 520 +/- 330 pmol/L; P < 0.05). Aldosterone was unresponsive (rose by <50%) to AII in all subjects. Day curve studies (blood collected every 2 h for 24 h; n = 2 mild and 7 severe) demonstrated abnormal regulation of aldosterone by ACTH rather than by AII in both groups. In conclusion, in this series of patients with FH-I, males had more severe hypertension, and the degree of hybrid gene-induced aldosterone overproduction may have contributed to the severity of hypertension.

Treatment of familial hyperaldosteronism type I: only partial suppression of adrenocorticotropin required to correct hypertension.

In familial hyperaldosteronism type I, inheritance of a hybrid 11beta-hydroxylase/aldosterone synthase gene leads to ACTH-regulated overproduction of aldosterone (causing hypertension) and of "hybrid" steroids, 18-hydroxy- and 18-oxo-cortisol. To determine whether complete suppression of the hybrid gene is necessary to normalize blood pressure, we sought evidence of persisting expression in eight patients who were rendered normotensive for 1.3-4.5 yr by glucocorticoid treatment. At the time of the study, six patients were receiving dexamethasone (0.125-0.25 mg/day) and two patients were taking prednisolone (2.5 or 5 mg/day). Urinary 18-oxo-cortisol levels during treatment demonstrated close correlation with mean "day curve" (blood collected every 2 h for 24 h) cortisol (r = 0.74), consistent with regulation by ACTH. Although urinary 18-oxo-cortisol levels were lower during than before treatment (mean 12.6 +/- 2.4 SEM vs. 35.0 +/- 5.6 nmol/mmol creatinine; P < 0.01), they remained above normal (0.8-5.2 nmol/mmol creatinine) in all eight patients. Although mean upright plasma potassium levels during treatment were higher, aldosterone levels lower, PRA levels higher, and aldosterone to PRA ratios lower than before treatment, PRA levels were uncorrected (< 13 pmol/L x min) and aldosterone to PRA ratios were uncorrected (>65) during treatment in four patients. For each of the eight patients, day curve aldosterone levels during treatment correlated more tightly with cortisol (mean r for the eight patients, 0.87 +/- 0.05 SEM) than with PRA (mean r = 0.36 +/- 0.10 SEM). Hence, control of hypertension by glucocorticoid treatment was associated, in all patients, with only partial suppression of ACTH-regulated hybrid steroid and aldosterone production. Normalization of urinary hybrid steroid levels and abolition of ACTH-regulated aldosterone production is not a requisite for hypertension control and, if used as a treatment goal, may unnecessarily increase the risk of Cushingoid side effects.

Biochemical evidence of aldosterone overproduction and abnormal regulation in normotensive individuals with familial hyperaldosteronism type I.

We examined in detail biochemical characteristics of 10 normotensive individuals (6 females; age range, 11-43 yr) with glucocorticoid-suppressible hyperaldosteronism (familial hyperaldosteronism type I) in an attempt to understand the development of hypertension in this disorder. All were normokalemic (median plasma potassium, 3.7 +/- 0.4 mmol/L SD), and upright plasma aldosterone levels (478 +/- 333 pmol/L) were within the normal range (140-1110 pmol/L) in nine subjects. However, upright PRA levels (3.3 +/- 30.5 pmol/L x min) were suppressed (<13 pmol/L x min), and the aldosterone to PRA ratio (169.0 +/- 308.3) was elevated (>65) in all but one subject. All subjects had elevated 24-h urinary levels of 18-oxo-cortisol (34.3 +/- 11.2 nmol/mmol creatinine; normal range, 0.8-6.5 nmol/mmol creatinine). Plasma aldosterone failed to rise by at least 50% during 2 h of upright posture in five of seven subjects, or during a 1-h infusion of angiotensin II (2 ng/kg x min) in each of six subjects so studied. Serial, second-hourly (day-curve) aldosterone levels correlated tightly with cortisol (r = 0.79-0.97, P < 0.01 to 0.001), but not with PRA (r = 0.13-0.40, not significant) levels in each of six subjects, and plasma aldosterone suppressed to less than 110 pmol/L during 4 days of dexamethasone administration (0.5 mg 6 hourly) in each of two studied, consistent with ACTH-regulated aldosterone production. In conclusion, biochemical evidence of excessive, abnormally regulated aldosterone production is present not only in hypertensive individuals with familial hyperaldosteronism type I, but also in those who are normotensive. The absence of hypertension in such individuals, therefore, cannot be attributed to lack of biochemical expression of the hybrid gene.

Familial corticosteroid-binding globulin deficiency due to a novel null mutation: association with fatigue and relative hypotension.

Corticosteroid-binding globulin is a 383-amino acid glycoprotein that serves a hormone transport role and may have functions related to the stress response and inflammation. We describe a 39-member Italian-Australian family with a novel complete loss of function (null) mutation of the corticosteroid-binding globulin gene. A second, previously described, mutation (Lyon) segregated independently in the same kindred. The novel exon 2 mutation led to a premature termination codon corresponding to residue -12 of the procorticosteroid-binding globulin molecule (c.121G-->A). Among 32 family members there were 3 null homozygotes, 19 null heterozygotes, 2 compound heterozygotes, 3 Lyon heterozygotes, and 5 individuals without corticosteroid-binding globulin mutations. Plasma immunoreactive corticosteroid-binding globulin was undetectable in null homozygotes, and mean corticosteroid-binding globulin levels were reduced by approximately 50% at 18.7 +/- 1.3 microg/ml (reference range, 30-52 microg/ml) in null heterozygotes. Morning total plasma cortisol levels were less than 1.8 microg/dl in homozygotes and were positively correlated to the plasma corticosteroid-binding globulin level in heterozygotes. Homozygotes and heterozygote null mutation subjects had a high prevalence of hypotension and fatigue. Among 19 adults with the null mutation, the systolic blood pressure z-score was 12.1 +/- 3.5; 11 of 19 subjects (54%) had a systolic blood pressure below the third percentile. The mean diastolic blood pressure z-score was 18.1 +/- 3.4; 8 of 19 subjects (42%) had a diastolic blood pressure z-score below 10. Idiopathic chronic fatigue was present in 12 of 14 adult null heterozygote subjects (86%) and in 2 of 3 null homozygotes. Five cases met the Centers for Disease Control criteria for chronic fatigue syndrome. Fatigue questionnaires revealed scores of 25.1 +/- 2.5 in 18 adults with the mutation vs. 4.2 +/- 1.5 in 23 healthy controls (P < 0.0001). Compound heterozygosity for both mutations resulted in plasma cortisol levels comparable to those in null homozygotes. Abnormal corticosteroid-binding globulin concentrations or binding affinity may lead to the misdiagnosis of isolated ACTH deficiency. The mechanism of the association between fatigue and relative hypotension is not established by these studies. As idiopathic fatigue disorders are associated with relatively low plasma cortisol, abnormalities of corticosteroid-binding globulin may be pathogenic.

Clinical, biochemical and genetic approaches to the detection of familial hyperaldosteronism type I.

AIM: Since detection of familial hyperaldosteronism type I (glucocorticoid-suppressible hyperaldosteronism) allows specific treatment of hypertension with dexamethasone, we compared clinical, biochemical and genetic approaches to detection. PATIENTS AND METHODS: We studied 22 affected patients, 21 from a single, large family and an additional adopted male. Plasma aldosterone, plasma renin activity and urinary 18-oxo-cortisol were measured by radioimmunoassay. The hybrid gene was demonstrated using either Southern blotting or a long polymerase chain reaction technique. RESULTS: Thirteen out of 22 (59%) patients with familial hyperaldosteronism type I, but only four out of 12 (33%) under 20 years of age, were hypertensive. Plasma potassium and aldosterone were each normal in 20 out of 22 (91%), and unhelpful in diagnosis. Plasma renin activity, the aldosterone: plasma renin activity ratio and 18-oxo-cortisol were more sensitive, being abnormal in 20 out of 22 (91%), 19 out of 22 (86%) and 20 out of 20 (100%) patients, respectively. Aldosterone was unresponsive (<50% rise) to 2 h of upright posture following overnight recumbency in 15 out of 15 (100%) patients studied, and to angiotensin II infusion (2 ng/kg per min for 1 h) in 14 out of 14 patients (100%). Whereas all the abovementioned abnormalities are also characteristic of angiotensin II-unresponsive aldosterone-producing adenoma, marked aldosterone suppression following 4 days of dexamethasone (0.5 mg every 6 h) was sensitive and specific for familial hyperaldosteronism type I (n = 11). The hybrid gene was detectable in peripheral blood leucocyte DNA in all 22 affected patients by Southern blotting, and by a faster, long polymerase chain reaction method developed in our laboratory, both methods requiring only a single blood collection. CONCLUSIONS: Should studies in other families confirm its universal applicability, long polymerase chain reaction should prove to be the most practical means of detecting familial hyperaldosteronism type I in laboratories equipped with this technique.

A comparison of cardiovascular and catecholamine responses to three stimuli in mild hypertension.

In five males with mild essential hypertension, simultaneous hemodynamic and arterial and venous plasma catecholamine responses to three stimulation tests (mental arithmetic, isometric handgrip exercise, and cold) were studied. Plasma norepinephrine (NE), epinephrine (EPI), and dopamine (DA) were measured radioenzymatically. Isometric exercise was the best stimulus for systolic and diastolic blood pressure and NE. Mental arithmetic produced the highest levels of plasma EPI, but there was great intersubject variability. Dopamine levels did not increase with any of these stimuli. Consistent arterio-venous differences across the forearm were seen for EPI but not NE, consistent with local production of NE. Isometric exercise produced the closest correlations between peripheral plasma catecholamine levels, blood pressure, and heart rate. Good correlations were seen with mental arithmetic, but with the stimulus of cold correlation was poor.

Markers for monitoring overtraining and recovery.

Physiological and mood state parameters were monitored during a 6-month swimming season in an attempt to determine markers of overtraining and recovery. Fourteen elite male and female swimmers were tested early-, mid-, and late-season and shortly before and after major competition. Training details and subjective ratings of well-being were compiled by the athletes in daily logs. Three swimmers were classified as stale based upon performance deterioration and prolonged, high fatigue levels. Staleness scores were calculated for each athlete using performance change from early- to late-season and daily fatigue ratings for the season. Regression analysis revealed a battery of well-being ratings which predicted staleness scores, accounting for 76% of the variance. The late-season stress ratings and plasma catecholamine levels at rest predicted staleness scores, accounting for 85% of the variance. During tapering, well-being ratings predicted improvement in competitive performance, accounting for 72% of the variance of the improvement in race times from previous best times. It was concluded that self-reported ratings of well-being may provide an efficient means of monitoring both overtraining and recovery; plasma catecholamine levels at rest may provide an additional objective tool for diagnosis.

Hormonal responses of elite swimmers to overtraining.

Fourteen elite swimmers had measurements of stress hormones taken at five points during a 6-month season: early-, mid- and late-season, during tapering for National Trials, and 1-3 d after the Trials. Training details and subjective ratings of fatigue were recorded daily in log books. Plasma norepinephrine and epinephrine concentrations were significantly correlated with swim training volume (r = 0.37 and 0.33, respectively, P < 0.05 for each). No significant differences were seen in norepinephrine or cortisol concentrations at the five sampling times. Epinephrine levels were significantly lower (P < 0.05) after competition compared with values early in the season and shortly before competition. Symptoms of the overtraining syndrome were identified in three of the swimmers, based on performance decrements and high, prolonged levels of fatigue. In these three swimmers, norepinephrine levels tended to be higher than those of the other swimmers from mid-season onward and were significantly higher (P < 0.01) during tapering. If these findings can be confirmed in larger numbers and different types of athletes, norepinephrine level may provide a useful marker of the overtraining syndrome.

Hormonal, immunological, and hematological responses to intensified training in elite swimmers.

The purpose of this study was to compare the responses of selected hormonal, immunological, and hematological variables in athletes showing symptoms of overreaching with these variables in well-trained athletes during intensified training. Training volume was progressively increased over 4 wk in 24 elite swimmers (8 male, 16 female); symptoms of overreaching were identified in eight swimmers based on decrements in swim performance, persistent high ratings of fatigue, and comments in log books indicating poor adaptation to the increased training. Urinary excretion of norepinephrine was significantly lower (P < 0.05, post hoc analysis) in overreached (OR) compared with well-trained (WT) swimmers throughout the 4 wk. There were no significant differences between OR and WT swimmers for other variables including: concentrations of plasma norepinephrine, cortisol, and testosterone, and the testosterone/cortisol ratio; peripheral blood leukocyte and differential counts, neutrophil/lymphocyte ratio, and CD4/CD8 cell ratio; serum ferritin and blood hemoglobin concentrations, erythrocyte number, hematocrit, and mean red cell volume (MCV). MCV increased significantly over the 4 wk in both groups, suggesting increased red blood cell turnover. These data show that, of the 16 hormonal, immunological, and hematological variables measured, urinary norepinephrine excretion appears to be the only one to distinguish OR from WT swimmers during short-term intensified training. Low urinary norepinephrine excretion was observed 2 to 4 wk before the appearance of symptoms of overreaching, suggesting the possibility that neuroendocrine changes may precede, and possibly contribute to, development of the overreaching/overtraining syndromes.

Increased plasma noradrenaline during adrenaline infusion in man.

Arterial and venous plasma noradrenaline in recumbent mild hypertensives, and in normotensives with one adrenal gland, increased significantly during infusion of adrenaline to achieve levels similar to those seen during mental arithmetic stress. Although decreased noradrenaline clearance has not been excluded as an explanation of increased plasma levels, these results are consistent with the hypothesis that physiological concentrations of adrenaline are capable of facilitating noradrenaline release in man.

Reduced adrenal secretory mass after unilateral adrenalectomy for aldosterone-producing adenoma may explain unexpected incidence of hypotension.

In a prospective study of 37 patients who had unilateral adrenalectomy for an aldosterone-producing adenoma, five of 33 (15%) were symptomatically hypotensive after at least 1 year, and eight of 29 (28%) who were observed 3, 6, 12, 18 and 24 months after the operation showed 2-year blood pressures below the fifth percentile for age- and sex-matched controls. Postoperatively, plasma aldosterone was lower, and plasma renin activity higher than in controls, these differences being more marked in the hypotensive group. Pre-operatively elevated atrial natriuretic factor fell to levels lower than in controls. These serial changes in volume-regulatory hormones are consistent with chronic hypovolaemia, due to relative hypoaldosteronism. Plasma cortisol was lower 6 months after the operation and plasma adrenaline levels fell by half. A reduced adrenocortical (aldosterone and cortisol) and adrenomedullary (adrenaline) secretory mass may play a role in the hypotension observed after unilateral adrenalectomy.

Fibroblast growth factor receptor 1 is a key regulator of early adipogenic events in human preadipocytes.

Cell number is an important determinant of adipose tissue mass, and the coordinated proliferation and differentiation of preadipocytes into mature lipid-laden adipocytes underpins the increased adipose tissue mass associated with obesity. Despite this, the molecular cues governing such adipose tissue expansion are poorly understood. We previously reported that fibroblast growth factor-1 (FGF-1) promotes both proliferation and differentiation of human preadipocytes and that the major adipogenic effect of FGF-1 occurs during proliferation, priming the cells for adipose conversion. In the current study, we examined whether this effect was linked to the mitogenic action of FGF-1 by investigating the mitogenic and adipogenic potential of other growth factors, platelet-derived growth factor (PDGF; AA and BB) and vascular endothelial growth factor. Although PDGF-AA and PDGF-BB showed comparable mitogenic potential to FGF-1, only FGF-1 treatment resulted in priming and subsequent differentiation. Pharmacological inhibition of FGF receptor (FGFR) tyrosine kinase activity, using the FGFR-specific inhibitors PD-173074 and SU-5402, revealed an obligate requirement for FGFR activity in these processes. A combination of biochemical and genetic approaches revealed an important role for FGFR1. Knock down of FGFR1 expression by small-interfering RNA reduced FGF-1-stimulated signaling events, proliferation, and priming. Together these data highlight the unique nature of the role of FGF-1 during the earliest stages of adipogenesis and establish a role for FGFR1 in human adipogenesis, identifying FGFR1 as a potential therapeutic target to reduce obesity.

Clonidine suppression test reliably differentiates phaeochromocytoma from essential hypertension.

1. Clonidine resulted in significant suppression of both noradrenaline (NA) and adrenaline (ADR) in essential hypertensives (EHT) without any false positive findings. That is, every patient who failed to suppress had phaeochromocytoma (PH). 2. The clonidine suppression test (CST) produced minimal suppression of NA in NA-secreting PH (NA-PH) and correctly identified two NA-PH with normal basal plasma NA. 3. In ADR-secreting PH (ADR-PH) the CST did not result in significant suppression of ADR levels, whether elevated or normal basally. 4. The CST proved to be an accurate discriminator of PH from other forms of hypertension.

Response of atrial natriuretic peptide to adrenaline and noradrenaline infusion in man.

1. Atrial natriuretic peptide (ANP) levels were significantly increased during both adrenaline and noradrenaline infusions, in the physiological range, in normal subjects and in patients with essential hypertension. 2. During adrenaline infusion significant increases in both circulating adrenaline and noradrenaline levels were observed. Mean arterial pressure was unaltered. Changes in heart rate were not significant. 3. During noradrenaline infusion, significant increases in circulating noradrenaline and mean arterial pressure were also observed. Heart rate and plasma adrenaline levels were unaltered. 4. Fluctuations in sympathetic nervous system activity may be involved in the regulation of ANP via adrenoceptor stimulated release of ANP. Other known regulators such as atrial stretch and increasing heart rate may modify this response.

Effect of positive family history of hypertension on the blood pressure and catecholamine responses to a 6 hour adrenaline infusion.

1. The effects of 6 h infusion of adrenaline (INF-A) or dextrose (INF-D) and of post-infusion cold pressor test (CPT) were compared in normal subjects, with (FH+) and without (FH-) a family history of hypertension. 2. Increased urinary excretion rates suggested facilitated noradrenaline (NA) release during and after INF-A in both FH+ and FH-. 3. Urinary adrenaline (UADR) excretion increased during INF-A, as expected, and was also slightly higher after INF-A than INF-D. 4. The effect of INF-A on systolic blood pressure (SBP) was greater in FH- than in FH+ but diastolic blood pressure (DBP) did not fall as quickly with nocturnal recumbency after INF-A in FH+. 5. A significantly greater response in plasma NA to CPT was seen in FH+ than in FH- after INF-A. A similar trend was also seen after INF-D. 6. Increases in DBP due to CPT were higher in FH+ than in FH- after both infusions. 7. This study provides evidence of increased noradrenergic activity during and after INF-A, and also of a difference in response to sympathetic stimulation between FH+ and FH-.

Effects of repeated doses of pseudoephedrine on blood pressure and plasma catecholamines in normal subjects and in patients with phaeochromocytoma.

1. Increases in blood pressure (BP) and in plasma noradrenaline concentration (NA) were observed after two doses of a non-prescription decongestant containing pseudoephedrine (PE) in two of three patients with phaeochromocytoma, before but not after removal of the tumour. The pressor response was terminated by oral phenoxybenzamine, and modified by prior exposure to this drug. 2. In eight normal subjects administration of the same two doses prevented falls in BP and in NA usually seen with prolonged recumbency, but neither BP nor NA increased. However, a pressor response was observed in a normal subject with a strong family history of hypertension. 3. Exposure to PE in non-prescription decongestants is not without risk in hypertension.

Evidence for presynaptic beta-adrenoceptor stimulation 24 hours after a 6 hour adrenaline infusion.

1. The effects of 6 h infusions of adrenaline (INF-A) and dextrose (INF-D) were compared in nine normal subjects. 2. A significant increase in systolic blood pressure was observed during INF-A compared with INF-D and, 24 h after infusion, diastolic blood pressure was higher after INF-A than after INF-D. 3. Heart rate (HR) was significantly higher during INF-A than during INF-D. 4. As expected, plasma ADR increased significantly during INF-A but, unexpectedly, remained elevated 60 min post infusion compared with INF-D. Levels during activity the next morning were somewhat higher after INF-A, but not significantly different from INF-D. 5. Plasma NA increased transiently during INF-A and decreased during INF-D. Urinary NA was significantly higher during INF-A than during INF-D, and insignificantly higher during overnight recumbency, consistent with enhanced noradrenergic transmission.

Infusions of adrenaline stimulate noradrenergic transmission in man, but adrenaline is not released later as a co-transmitter.

A pre-junctional beta-adrenoceptor facilitating noradrenergic transmission may be affected by elevations in circulating adrenaline, and represent a mechanism whereby mental stress might predispose to hypertension. The proposition that circulating adrenaline can be taken up into noradrenergic nerve terminals and later co-released with noradrenaline in response to an appropriate stimulus was examined. The effects of upright posture, before and after a 60 min adrenaline infusion were as follows: (1) Changes in heart rate and diastolic blood pressure were not augmented. (2) Plasma noradrenaline response was not increased. (3) Plasma adrenaline basally and in response to posture remained low. (4) Radiolabelled adrenaline disappeared from the circulation on cessation of infusion, and did not reappear in response to posture or isometric exercise. While adrenaline infusion again increased noradrenaline, we found no evidence of subsequent adrenaline release in response to noradrenergic stimulation. These studies do not exclude adrenaline uptake and re-release in amounts sufficient to stimulate the prejunctional beta-adrenoceptor, but insufficient to reach the circulation after local metabolism.

Phaeochromocytomas secreting adrenaline but not noradrenaline do not cause hypertension and require precise adrenaline measurement for diagnosis.

1. Urinary noradrenaline (NA) and adrenaline (ADR) determinations are a more sensitive index than plasma measurements for the diagnosis of phaeochromocytoma (phaeo). 2. Even though urinary NA excretion serve as a sufficient single diagnostic test for the majority of phaeos, it is necessary to measure urinary ADR excretion if ADR-only secreting phaeos are not to be missed, particularly in patients with multiple endocrine neoplasia (MEN) syndrome. 3. The clonidine suppression test confirmed all tumour diagnoses, and in this series was not responsible for any false negative or false positive results.

Haemoglobins in cattle and buffalo. Haemoglobin types of Bos taurus, Bos indicus, Bos banteng and Bubalis bubalis in northern Australia.

The frequency of haemoglobin types in several major breeds of cattle in northern Austrailia was determined. In all Boss taurus cattle examined only the three common bovine haemoglobin types (AA, AB, BB) were found. F2 Africander cross-breeds showed only AA patterns. The frequency of haemoglobin B was significantly higher in Bos indicus type cattle than in Bos taurus breeds. In the pure breed Banteng cattle (Bos banteng) three genotypes (BB, CB, CC) were present. The eleven buffaloes types each showed two haemoglobins (A1 and A2) in proporotions of 71 to 29 respectively.